1) Cancer cells exhibit altered metabolism compared to normal cells in order to support their high rates of proliferation. This altered metabolism represents an attractive therapeutic target, but selectively targeting cancer cell metabolism while sparing normal cells is challenging.
2) Some of the earliest effective cancer therapies, such as antifolate drugs, target the specific metabolic needs of cancer cells. Targeting cancer cell metabolism remains a promising strategy.
3) Research into how changes in cell metabolism promote tumor growth has accelerated in recent years, refocusing efforts on targeting the metabolic dependencies of cancer cells as a selective anticancer approach.
Cancer cells exhibit abnormal metabolism known as the Warburg effect, in which they rely primarily on aerobic glycolysis rather than oxidative phosphorylation to generate energy. This results in lactate production even in the presence of oxygen. Genetic mutations in pathways such as PI3K, VHL, and MYC influence cancer cell metabolism by increasing glucose uptake and glycolytic enzyme expression. Abnormal metabolism in cancer is a potential therapeutic target, and imaging techniques like PET scans using fluorine-18 labeled glucose can detect changes in cancer cell metabolism in patients undergoing treatment.
Cancer metabolism lecture, Hood College (10-18-10)James Gould, PhD
Cancer cells alter their metabolism to favor aerobic glycolysis over oxidative phosphorylation even in the presence of oxygen (known as the Warburg effect). This metabolic reprogramming is driven by genetic mutations and changes in transcription factors like c-MYC, HIF-1, and loss of p53 function. Upregulation of glycolytic enzymes and transporters by these transcription factors increases glucose uptake and lactate production. This altered metabolism provides advantages for cancer cell growth and survival in the low-oxygen tumor microenvironment.
here is some information about autophagy, how it happend, when it happend and it's mechanism.
and some information about it's effect on cancer and some disorders.
Cancer cells exhibit altered metabolism compared to normal cells. They metabolize glucose to lactate through aerobic glycolysis even when oxygen is present, known as the Warburg effect. Normal cells only undergo glycolysis and produce lactate under low oxygen conditions. Cancer cells also rely on glutaminolysis and have hyperpolarized mitochondria. Inhibiting key steps in glycolysis and mitochondrial metabolism may be potential anti-tumor strategies. Targeting glucose transport, pyruvate oxidation, and mitochondrial metabolism are emerging areas of research.
The document discusses the Warburg effect, where cancer cells preferentially use glycolysis over oxidative phosphorylation to generate energy, even in the presence of oxygen. This allows cancer cells to rapidly proliferate by generating ATP and biomass through glycolysis. The effect occurs because cancer cells overexpress hypoxia-inducible factor 1, increasing glycolytic enzymes and decreasing mitochondrial function. While the exact cause is still unknown, the Warburg effect provides cancer cells a growth advantage and is exploited in PET scanning and as a target for potential anticancer drugs.
Cancer cells have altered metabolism compared to normal cells. They rely more on glycolysis even in the presence of oxygen (Warburg effect). This produces less ATP but helps cancer cells proliferate rapidly. Glutamine can also be used as an energy source. Targeting cancer cell metabolism through drugs like dichloroacetate is a potential treatment strategy. Cancers are heterogeneous so their metabolic profiles vary between cancer types and individual cells.
Cancer cells exhibit altered metabolism compared to normal cells. They metabolize glucose to lactate through aerobic glycolysis even when oxygen is present, known as the Warburg effect. This was discovered by Otto Warburg. Cancer cells rely more on glycolysis than oxidative phosphorylation in the mitochondria to generate energy. Targeting glycolysis and mitochondrial metabolism in cancer cells may be a promising strategy to inhibit tumor growth by depriving them of nutrients and energy.
Use slideshow after downloading for better viewing. The slides cover altered metabolism in cancer with a focus on Warburg effect and drug targeting of metabolic pathways for cancer treatment.
Prepared in Oct 2014
Cancer cells exhibit abnormal metabolism known as the Warburg effect, in which they rely primarily on aerobic glycolysis rather than oxidative phosphorylation to generate energy. This results in lactate production even in the presence of oxygen. Genetic mutations in pathways such as PI3K, VHL, and MYC influence cancer cell metabolism by increasing glucose uptake and glycolytic enzyme expression. Abnormal metabolism in cancer is a potential therapeutic target, and imaging techniques like PET scans using fluorine-18 labeled glucose can detect changes in cancer cell metabolism in patients undergoing treatment.
Cancer metabolism lecture, Hood College (10-18-10)James Gould, PhD
Cancer cells alter their metabolism to favor aerobic glycolysis over oxidative phosphorylation even in the presence of oxygen (known as the Warburg effect). This metabolic reprogramming is driven by genetic mutations and changes in transcription factors like c-MYC, HIF-1, and loss of p53 function. Upregulation of glycolytic enzymes and transporters by these transcription factors increases glucose uptake and lactate production. This altered metabolism provides advantages for cancer cell growth and survival in the low-oxygen tumor microenvironment.
here is some information about autophagy, how it happend, when it happend and it's mechanism.
and some information about it's effect on cancer and some disorders.
Cancer cells exhibit altered metabolism compared to normal cells. They metabolize glucose to lactate through aerobic glycolysis even when oxygen is present, known as the Warburg effect. Normal cells only undergo glycolysis and produce lactate under low oxygen conditions. Cancer cells also rely on glutaminolysis and have hyperpolarized mitochondria. Inhibiting key steps in glycolysis and mitochondrial metabolism may be potential anti-tumor strategies. Targeting glucose transport, pyruvate oxidation, and mitochondrial metabolism are emerging areas of research.
The document discusses the Warburg effect, where cancer cells preferentially use glycolysis over oxidative phosphorylation to generate energy, even in the presence of oxygen. This allows cancer cells to rapidly proliferate by generating ATP and biomass through glycolysis. The effect occurs because cancer cells overexpress hypoxia-inducible factor 1, increasing glycolytic enzymes and decreasing mitochondrial function. While the exact cause is still unknown, the Warburg effect provides cancer cells a growth advantage and is exploited in PET scanning and as a target for potential anticancer drugs.
Cancer cells have altered metabolism compared to normal cells. They rely more on glycolysis even in the presence of oxygen (Warburg effect). This produces less ATP but helps cancer cells proliferate rapidly. Glutamine can also be used as an energy source. Targeting cancer cell metabolism through drugs like dichloroacetate is a potential treatment strategy. Cancers are heterogeneous so their metabolic profiles vary between cancer types and individual cells.
Cancer cells exhibit altered metabolism compared to normal cells. They metabolize glucose to lactate through aerobic glycolysis even when oxygen is present, known as the Warburg effect. This was discovered by Otto Warburg. Cancer cells rely more on glycolysis than oxidative phosphorylation in the mitochondria to generate energy. Targeting glycolysis and mitochondrial metabolism in cancer cells may be a promising strategy to inhibit tumor growth by depriving them of nutrients and energy.
Use slideshow after downloading for better viewing. The slides cover altered metabolism in cancer with a focus on Warburg effect and drug targeting of metabolic pathways for cancer treatment.
Prepared in Oct 2014
The document summarizes Otto Warburg's discovery of the Warburg effect. Warburg showed in the 1920s that tumor cells metabolize glucose to lactate at a much higher rate than normal cells, even in the presence of oxygen. This is known as aerobic glycolysis or the Warburg effect. The document then discusses various causes and mechanisms of the Warburg effect, including mutations, hypoxia in tumor microenvironments, overexpression of glycolytic enzymes, and mitochondrial dysfunction in cancer cells. It also notes some characteristics of the Warburg effect such as cancer cell adaptations to hypoxia and maintenance of an intracellular alkaline pH.
The PI3K-Akt-mTOR pathway is an intracellular signal transduction pathway that promotes metabolism, proliferation, cell survival, growth and angiogenesis. Key components include receptor tyrosine kinases, PI3K, PIP2, PIP3, and Akt. Akt is activated by phosphorylation and regulates various proteins involved in functions like cell growth. Dysregulation of this pathway can lead to cancer due to abnormal cell proliferation and is associated with neurodevelopmental disorders.
Cellular Signaling Pathways have direct implications on our understanding of tumor cell behavior. A general overview is presented here followed by a brief discussion of some of the major pathways currently implicated in cancer progression : Ras/RAF/MAP kinase pathway and PI3K/AKT/mTOR pathway s
The Warburg effect refers to cancer cells predominantly producing energy by a high rate of glycolysis followed by lactic acid fermentation in the cytosol, rather than by a comparatively low rate of glycolysis followed by oxidation of pyruvate in mitochondria as in most normal cells. Otto Warburg observed that solid tumor cells metabolize glucose to lactate at a much higher rate than normal tissues, even in the presence of oxygen. This metabolic shift is caused by mitochondrial defects, hypoxia within tumors, oncogenic signaling, and altered expression of metabolic enzymes. Understanding the Warburg effect has led to the development of novel anti-cancer therapies targeting tumor cell glycolysis.
An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are mutated or expressed at high levels. Most normal cells undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered.
Signal transduction proteins and pathways in oncogenesisShashidhara TS
1. The document discusses various signal transduction proteins and pathways that are involved in oncogenesis, including growth factor receptors, Ras, PI3K/Akt, JAK/STAT, and cyclic AMP signaling pathways.
2. Mutations in these proteins and pathways, such as activating mutations in Ras, receptor tyrosine kinases, JAK2, and STATs can lead to constitutive signaling and uncontrolled cell growth.
3. Targeting key nodes in these altered pathways, such as BCR-ABL fusion protein, mutant Ras, PI3K, and JAK2, may provide opportunities for targeted cancer therapies.
The p53 gene is a tumor suppressor gene that regulates the cell cycle and prevents tumor formation. It acts as the "guardian of the genome" by inducing cell cycle arrest or apoptosis in damaged cells. p53 is commonly mutated in cancer, inactivating its normal functions and allowing damaged cells to continue dividing. When p53 is mutated, DNA damage fails to trigger cell cycle arrest, potentially leading to neoplastic transformation. The document discusses p53's role in DNA repair, apoptosis, and cell cycle regulation as well as how it is inactivated through mutations and the cancers most associated with p53 mutations, such as breast, colorectal, liver, lung, and ovarian cancers.
Majority of cancer lead by point mutation in p53 gene. which is also known as "guardian of genome". this mutation leads conversion of normal cell into cancerous cell.
Genomic instability refers to changes in chromosome structure and number that can lead to cancer. It is caused by failures in DNA replication, damage sensing and repair, and cell cycle checkpoints. There are several types of genetic instability, including chromosomal instability (CIN), microsatellite instability (MIN), and DNA replication errors. CIN results in chromosome gains and losses, while MIN causes repetitive DNA expansions and contractions. Genomic instability can arise from defects in DNA damage response genes like p53 and ATM, problems with DNA replication, fragile sites in the genome, and DNA secondary structures. While genetic instability promotes evolution, it also contributes to pathological conditions like cancer by enabling the accumulation of mutations needed for malignant transformation.
This document summarizes key concepts regarding oncogenes:
1. Oncogenes are genes that can trigger cancer development through viral insertion or mutation of normal cellular genes.
2. Early retroviruses like RSV were found to contain viral oncogenes like v-src that caused cancer upon infection.
3. Normal cellular genes called proto-oncogenes were later discovered that are homologous to viral oncogenes and can become activated by mutations to drive cancer. Common mutations include point mutations, gene amplifications, and chromosomal translocations.
Structure, functions and folding problems of proteinRawat DA Greatt
This document provides an overview of protein structure and folding. It discusses the four levels of protein structure - primary, secondary, tertiary, and quaternary. Common secondary structures like alpha helices and beta sheets are described. The document also introduces concepts like the Ramachandran plot, which maps allowed phi and psi dihedral angles in protein backbones. Protein folding and factors involved like molecular chaperones are also summarized. Disorders resulting from changes in protein conformation are briefly mentioned.
1. Lysozyme attaches to bacterial cell walls and uses its Glu 35 residue to transfer a proton to cleave the bond between the D- and E-rings of the cell wall, forming an oxonium ion transition state.
2. The Asp 52 carboxylate group then nucleophilically attacks the electron-poor carbon of the D-ring to form a glycosyl-enzyme intermediate.
3. Hydrolysis of this intermediate by Glu 35, forming another transition state, completes the catalytic cycle and releases the D-ring product.
1) Tumor suppressor genes normally apply brakes to cell proliferation through proteins that form checkpoints to prevent uncontrolled growth. Loss of function of these genes allows tumor development.
2) The proteins encoded by tumor suppressor genes regulate cell cycle control, apoptosis, and cell survival/growth through mechanisms like transcription factors, cell cycle inhibitors, and DNA damage response.
3) Famous tumor suppressor genes include RB, p53, APC, and WT1. Mutation of both copies is required for loss of function, leading to cancers like retinoblastoma, Li-Fraumeni syndrome, colon cancer, and Wilms tumor.
MicroRNAs (miRNAs) are small non-coding RNAs that play important gene regulatory roles in eukaryotic cells. They are approximately 22 nucleotides in length and are transcribed from independent genes or introns, then processed through a biogenesis pathway before targeting mRNAs for silencing or degradation. MiRNAs regulate genes involved in development, metabolism, and diseases like cancer. Their expression and function is tightly controlled through transcriptional and post-transcriptional mechanisms in order to influence protein expression levels. While much progress has been made in understanding miRNAs, further study is still needed to elucidate their complex regulatory networks and roles in development and disease.
This document summarizes the structure and function of phospholipids and glycolipids. It describes that phospholipids are composed of a phosphate group attached to diacylglycerol or sphingosine, making them amphipathic. There are two main classes - phosphoglycerides which use glycerol as a backbone, and sphingomyelin which uses sphingosine. Phospholipids are synthesized in the endoplasmic reticulum and degraded by phospholipases. Glycolipids are composed of carbohydrates attached to ceramides via glycosidic bonds. They include neutral cerebrosides and acidic gangliosides and sulfatides.
The document discusses the molecular mechanism of autophagy and its role in plants. It begins with an introduction to autophagy and discusses landmarks in the discovery of autophagy. It then covers the different classes of autophagy, genes and proteins involved, and the molecular mechanism. This includes discussion of the induction, expansion, and maturation steps. It also discusses selective autophagy and techniques to study autophagy. The document concludes by covering the physiological roles of autophagy in plants, including roles in nutrient starvation, oxidative stress response, development, pathogen response, and programmed cell death.
Presentation given by Dr. Karthikeyan at Department of Biochemistry, Maulana Azad Medical College.
Addition:
There are certain proteins which are degraded by proteasome without ubiquitin tag. one such example is ornithine decarboxylase - rate limiting enzyme of polyamine synthesis.
This document summarizes information about synzymes, which are artificial enzymes designed to mimic natural enzymes. It discusses the ideal characteristics of synzymes, such as having a hydrophobic binding site and catalytic group similar to enzymes. Approaches for designing synzymes include using cyclodextrins or cyclophanes to position catalytic groups to mimic enzyme active sites. Examples of reactions catalyzed by synzyme designs include palladium-based reactions and multi-step reactions through immobilizing multiple catalysts on polymers.
A novel use of biomarkers in the modeling of cancer activity based on the the...Kamyar Hedayat
Learn about a new approach to evaluating cancer that uses common biomarkers, but evaluates them using system theory. It looks as cancer as a whole-body disease expressed at the level of the cells, rather than a cellular disease expressed throughout the body.
Adsorption process for voc (volatile organic compounds copySaiful Islam
The document discusses the adsorption process for removing volatile organic compounds (VOCs) from air or gas streams. It defines adsorption and describes how VOCs accumulate on the surface of adsorbent materials like activated carbon. Fixed bed adsorption is commonly used, where the VOCs are removed as the contaminated air passes through a column packed with adsorbent. Key factors that influence the adsorption process include temperature, gas concentration, bed length, and regeneration of the adsorbent material. Common adsorbents for VOC removal include activated carbon beads and fibers, which can be used in continuous adsorption/desorption systems.
The document summarizes Otto Warburg's discovery of the Warburg effect. Warburg showed in the 1920s that tumor cells metabolize glucose to lactate at a much higher rate than normal cells, even in the presence of oxygen. This is known as aerobic glycolysis or the Warburg effect. The document then discusses various causes and mechanisms of the Warburg effect, including mutations, hypoxia in tumor microenvironments, overexpression of glycolytic enzymes, and mitochondrial dysfunction in cancer cells. It also notes some characteristics of the Warburg effect such as cancer cell adaptations to hypoxia and maintenance of an intracellular alkaline pH.
The PI3K-Akt-mTOR pathway is an intracellular signal transduction pathway that promotes metabolism, proliferation, cell survival, growth and angiogenesis. Key components include receptor tyrosine kinases, PI3K, PIP2, PIP3, and Akt. Akt is activated by phosphorylation and regulates various proteins involved in functions like cell growth. Dysregulation of this pathway can lead to cancer due to abnormal cell proliferation and is associated with neurodevelopmental disorders.
Cellular Signaling Pathways have direct implications on our understanding of tumor cell behavior. A general overview is presented here followed by a brief discussion of some of the major pathways currently implicated in cancer progression : Ras/RAF/MAP kinase pathway and PI3K/AKT/mTOR pathway s
The Warburg effect refers to cancer cells predominantly producing energy by a high rate of glycolysis followed by lactic acid fermentation in the cytosol, rather than by a comparatively low rate of glycolysis followed by oxidation of pyruvate in mitochondria as in most normal cells. Otto Warburg observed that solid tumor cells metabolize glucose to lactate at a much higher rate than normal tissues, even in the presence of oxygen. This metabolic shift is caused by mitochondrial defects, hypoxia within tumors, oncogenic signaling, and altered expression of metabolic enzymes. Understanding the Warburg effect has led to the development of novel anti-cancer therapies targeting tumor cell glycolysis.
An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are mutated or expressed at high levels. Most normal cells undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered.
Signal transduction proteins and pathways in oncogenesisShashidhara TS
1. The document discusses various signal transduction proteins and pathways that are involved in oncogenesis, including growth factor receptors, Ras, PI3K/Akt, JAK/STAT, and cyclic AMP signaling pathways.
2. Mutations in these proteins and pathways, such as activating mutations in Ras, receptor tyrosine kinases, JAK2, and STATs can lead to constitutive signaling and uncontrolled cell growth.
3. Targeting key nodes in these altered pathways, such as BCR-ABL fusion protein, mutant Ras, PI3K, and JAK2, may provide opportunities for targeted cancer therapies.
The p53 gene is a tumor suppressor gene that regulates the cell cycle and prevents tumor formation. It acts as the "guardian of the genome" by inducing cell cycle arrest or apoptosis in damaged cells. p53 is commonly mutated in cancer, inactivating its normal functions and allowing damaged cells to continue dividing. When p53 is mutated, DNA damage fails to trigger cell cycle arrest, potentially leading to neoplastic transformation. The document discusses p53's role in DNA repair, apoptosis, and cell cycle regulation as well as how it is inactivated through mutations and the cancers most associated with p53 mutations, such as breast, colorectal, liver, lung, and ovarian cancers.
Majority of cancer lead by point mutation in p53 gene. which is also known as "guardian of genome". this mutation leads conversion of normal cell into cancerous cell.
Genomic instability refers to changes in chromosome structure and number that can lead to cancer. It is caused by failures in DNA replication, damage sensing and repair, and cell cycle checkpoints. There are several types of genetic instability, including chromosomal instability (CIN), microsatellite instability (MIN), and DNA replication errors. CIN results in chromosome gains and losses, while MIN causes repetitive DNA expansions and contractions. Genomic instability can arise from defects in DNA damage response genes like p53 and ATM, problems with DNA replication, fragile sites in the genome, and DNA secondary structures. While genetic instability promotes evolution, it also contributes to pathological conditions like cancer by enabling the accumulation of mutations needed for malignant transformation.
This document summarizes key concepts regarding oncogenes:
1. Oncogenes are genes that can trigger cancer development through viral insertion or mutation of normal cellular genes.
2. Early retroviruses like RSV were found to contain viral oncogenes like v-src that caused cancer upon infection.
3. Normal cellular genes called proto-oncogenes were later discovered that are homologous to viral oncogenes and can become activated by mutations to drive cancer. Common mutations include point mutations, gene amplifications, and chromosomal translocations.
Structure, functions and folding problems of proteinRawat DA Greatt
This document provides an overview of protein structure and folding. It discusses the four levels of protein structure - primary, secondary, tertiary, and quaternary. Common secondary structures like alpha helices and beta sheets are described. The document also introduces concepts like the Ramachandran plot, which maps allowed phi and psi dihedral angles in protein backbones. Protein folding and factors involved like molecular chaperones are also summarized. Disorders resulting from changes in protein conformation are briefly mentioned.
1. Lysozyme attaches to bacterial cell walls and uses its Glu 35 residue to transfer a proton to cleave the bond between the D- and E-rings of the cell wall, forming an oxonium ion transition state.
2. The Asp 52 carboxylate group then nucleophilically attacks the electron-poor carbon of the D-ring to form a glycosyl-enzyme intermediate.
3. Hydrolysis of this intermediate by Glu 35, forming another transition state, completes the catalytic cycle and releases the D-ring product.
1) Tumor suppressor genes normally apply brakes to cell proliferation through proteins that form checkpoints to prevent uncontrolled growth. Loss of function of these genes allows tumor development.
2) The proteins encoded by tumor suppressor genes regulate cell cycle control, apoptosis, and cell survival/growth through mechanisms like transcription factors, cell cycle inhibitors, and DNA damage response.
3) Famous tumor suppressor genes include RB, p53, APC, and WT1. Mutation of both copies is required for loss of function, leading to cancers like retinoblastoma, Li-Fraumeni syndrome, colon cancer, and Wilms tumor.
MicroRNAs (miRNAs) are small non-coding RNAs that play important gene regulatory roles in eukaryotic cells. They are approximately 22 nucleotides in length and are transcribed from independent genes or introns, then processed through a biogenesis pathway before targeting mRNAs for silencing or degradation. MiRNAs regulate genes involved in development, metabolism, and diseases like cancer. Their expression and function is tightly controlled through transcriptional and post-transcriptional mechanisms in order to influence protein expression levels. While much progress has been made in understanding miRNAs, further study is still needed to elucidate their complex regulatory networks and roles in development and disease.
This document summarizes the structure and function of phospholipids and glycolipids. It describes that phospholipids are composed of a phosphate group attached to diacylglycerol or sphingosine, making them amphipathic. There are two main classes - phosphoglycerides which use glycerol as a backbone, and sphingomyelin which uses sphingosine. Phospholipids are synthesized in the endoplasmic reticulum and degraded by phospholipases. Glycolipids are composed of carbohydrates attached to ceramides via glycosidic bonds. They include neutral cerebrosides and acidic gangliosides and sulfatides.
The document discusses the molecular mechanism of autophagy and its role in plants. It begins with an introduction to autophagy and discusses landmarks in the discovery of autophagy. It then covers the different classes of autophagy, genes and proteins involved, and the molecular mechanism. This includes discussion of the induction, expansion, and maturation steps. It also discusses selective autophagy and techniques to study autophagy. The document concludes by covering the physiological roles of autophagy in plants, including roles in nutrient starvation, oxidative stress response, development, pathogen response, and programmed cell death.
Presentation given by Dr. Karthikeyan at Department of Biochemistry, Maulana Azad Medical College.
Addition:
There are certain proteins which are degraded by proteasome without ubiquitin tag. one such example is ornithine decarboxylase - rate limiting enzyme of polyamine synthesis.
This document summarizes information about synzymes, which are artificial enzymes designed to mimic natural enzymes. It discusses the ideal characteristics of synzymes, such as having a hydrophobic binding site and catalytic group similar to enzymes. Approaches for designing synzymes include using cyclodextrins or cyclophanes to position catalytic groups to mimic enzyme active sites. Examples of reactions catalyzed by synzyme designs include palladium-based reactions and multi-step reactions through immobilizing multiple catalysts on polymers.
A novel use of biomarkers in the modeling of cancer activity based on the the...Kamyar Hedayat
Learn about a new approach to evaluating cancer that uses common biomarkers, but evaluates them using system theory. It looks as cancer as a whole-body disease expressed at the level of the cells, rather than a cellular disease expressed throughout the body.
Adsorption process for voc (volatile organic compounds copySaiful Islam
The document discusses the adsorption process for removing volatile organic compounds (VOCs) from air or gas streams. It defines adsorption and describes how VOCs accumulate on the surface of adsorbent materials like activated carbon. Fixed bed adsorption is commonly used, where the VOCs are removed as the contaminated air passes through a column packed with adsorbent. Key factors that influence the adsorption process include temperature, gas concentration, bed length, and regeneration of the adsorbent material. Common adsorbents for VOC removal include activated carbon beads and fibers, which can be used in continuous adsorption/desorption systems.
The document discusses the relationship between cancer and cellular metabolism. It provides a brief history of how Otto Warburg first observed that cancer cells metabolize glucose differently than normal cells through aerobic glycolysis. More recently, there has been a renaissance in studying how oncogenes and tumor suppressor genes can alter cellular metabolism in cancer. The document then overviews key metabolic pathways and regulators that are altered in cancer, such as mutations in the TCA cycle enzymes IDH1 and IDH2. It describes techniques that can be used to study metabolism and cancer, such as analyzing mutations, gene expression, epigenetic changes, and cellular pathways. Throughout, it provides examples of studies investigating specific metabolic changes in cancer, such as how miRNAs
The Wnt signaling pathway controls cell-cell communication by transmitting signals from cell surface receptors to DNA expression in the nucleus. It regulates beta-catenin, which enters the nucleus to activate gene expression. Mutations that damage the pathway prevent proper control of beta-catenin, leading to over-expression of genes involved in diseases like cancer. Drugs targeting components of the Wnt pathway like beta-catenin show promise for treating cancers caused by alterations in this important signaling network.
The document describes the development of a multiplex panel to measure protein levels of HK2, PKM2, and LDHA in frozen tumor biopsies. Antibodies specific to these proteins were coupled to Luminex beads. Recombinant proteins were used to develop sandwich immunoassays and as calibrators. Sample handling procedures generated cytosolic and mitochondrial fractions from tumor tissues. The panel demonstrated proof-of-concept for monitoring PKM2 levels in cancer cell lines treated with PKM2 inhibitors in vitro.
Metabolomics & Lipidomics: From Discovery to Routine ApplicationsWaters Corporation
Presenter: Giuseppe Astarita, Ph.D., Principal Scientist, Waters Corp, Adjunct Professor, Georgetown University
A number of technological advancements have enhanced our ability to conduct metabolomics and lipidomics experiments. State-of-the-art chromatography, ionization sources, and MS technology combined with powerful informatics solutions provide a comprehensive set of tools to analyze complex mixtures of lipids and polar metabolites in biological samples. In this presentation, I will illustrate current workflows for metabolomics & lipidomics, including untargeted and targeted approaches, for discovery and routine applications.
This presentation was given at the 11th International Conference of the Metabolomics Society (Metabolomics 2015, #metsoc2015 on Twitter), June 29, 2015, in San Francisco.
Cancer cells are characterized by uncontrolled growth, immortality, and ability to invade tissues and metastasize. Cancer is caused by genetic mutations from radiation, chemicals, viruses, and oncogenes. Oncogenes activate cell growth, while tumor suppressor genes inhibit growth. Cancer cells evade growth suppression and express tumor markers, like AFP, CEA, PSA, and calcitonin, which are detected in screening and monitoring treatment effectiveness.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise boosts blood flow, releases endorphins, and promotes changes in the brain which help regulate emotions and stress levels.
Therapeutic targeting of cancer cell metabolism --role of metabolic enzymes, ...Younis I Munshi
The document summarizes recent developments in understanding the role of metabolic enzymes, oncogenes, and tumor suppressor genes in cancer progression and their potential as therapeutic targets. It discusses how cancer cells reprogram their metabolism to support uncontrolled proliferation. Key enzymes and pathways discussed include hexokinase, which phosphorylates glucose and fuels glycolysis; phosphofructokinase-2 and its role in regulating glycolytic flux; and pyruvate kinase isoforms PKM1 and PKM2 and their different functions in cancer metabolism. The document also examines how oncogenes like MYC and hypoxia-inducible factors influence these metabolic pathways to promote the Warburg effect and support tumor growth.
Cancer Cell Metabolism One Hallmark Many Faces Sabatini et al.pdfNguyenLinhNham
This document summarizes that cancer cells must alter their metabolism to support growth and proliferation in the same way that normal proliferating cells do. While the basic metabolic alterations are similar, cancer cells aberrantly drive these changes through genetic lesions and factors in the tumor microenvironment. The document discusses how proliferating cells increase glucose and glutamine uptake to fuel biosynthesis and meet energy demands. It also notes that while altered metabolism is a hallmark of cancer, there is heterogeneity in how individual tumors achieve metabolic reprogramming and in their specific metabolic dependencies or vulnerabilities. Understanding this complexity may help optimize strategies to target tumor metabolism therapeutically.
Cytokine Immunotherapy: A Forthcoming Visible Feature in Cancer TherapeuticsSachin K. S. Chauhan
The document discusses cytokine immunotherapy as a promising approach for cancer treatment. It notes that cytokines can stimulate the immune system to fight tumors, but that mono-cytokine therapy has limitations. Combined cytokine therapy or cytokine therapy combined with other treatments may be more effective by creating a specific immune response. The document advocates focusing research on combination therapies to help overcome drawbacks of traditional cancer treatments.
This document discusses tumor cell proliferation and immunotherapies for cancers. It covers the cell cycle phases and their implications for cancer therapy. Tumor growth can be altered by immunologic therapies, chemotherapy, hormones, radiation therapy and other factors. Biologic and targeted therapies that inhibit angiogenesis, growth factor receptors, and signaling pathways are described. Immunotherapy strategies including vaccines against HPV have shown success in preventing cervical cancer.
This document summarizes a study that investigated the effect of sodium dichloroacetate (DCA) on melanoma cells. The study found that DCA induced apoptosis in melanoma cells in a dose-dependent manner, with higher concentrations of DCA inducing apoptosis more rapidly. Leptin provided a protective effect against DCA-induced apoptosis. The results suggest that targeting cancer cell metabolism by switching them from glycolysis to oxidative phosphorylation through DCA treatment could be a potential therapeutic approach for treating melanoma.
This document discusses tumor cell proliferation and immunotherapy for cancers. It provides details on the cell cycle phases (M, G1, S, G2, G0) and how they relate to tumor growth and response to treatment. It also discusses cell kinetics, the growth fraction, and cancer stem cells. Targeted therapies discussed include those that inhibit angiogenesis by targeting VEGF, as well as EGFR inhibitors. Bevacizumab is highlighted as an anti-angiogenic therapy shown to improve outcomes for ovarian cancer both as a single agent and in combination with other drugs.
Crimson Publishers: Improved Version of Cancer Evo-Dev, a Novel Scientific Hy...CrimsonGastroenterology
Chronic but active inflammation, which is activated and maintained by stimulants such as infection and the interactions of stimulants with genetic predisposition, facilitates the occurrence and recurrence of cancers of various histotypes. Chronic inflammation, apparent or unapparent, is indispensible for the development of most malignancies, which has been clarified in hepatitis B virus (HBV)-induced hepatocellular carcinoma (HCC). Based on our previous work and the advances of researches on HBV-induced HCC and other inflammation-associated cancers, we presented the framework of a novel cancer theory termed Cancer Evolution and Development (Cancer Evo-Dev) [1-3]. Actually, Cancer Evo-Dev can be applied in cancers of many histotypes.
intrinsic signalling factors associated with cancer cells cell-fusion.pptxHammadAhmadCheema
1) Cancer cell fusion occurs when two or more cancer cells merge to form a hybrid cell. This can lead to increased tumor heterogeneity, metastatic potential, and drug resistance.
2) Dysfunctional p53, a tumor suppressor protein, may contribute to increased cancer cell fusion by affecting processes like cell cycle regulation and apoptosis.
3) Understanding the molecular mechanisms and implications of cancer cell fusion could reveal new therapeutic targets and strategies to inhibit fusion, hybrid cell formation, and tumor progression.
MULTIFACETED ROLES OF AUTOPHAGY IN CANCER & NEURODEGENERATIVE DISORDERSPHARMA IQ EDUCATION
1. What is Autophagy
2. Overview of the mechanisms lying behind autophagy
3. Mechanism of autophagy
4. Physiological role of autophagy
5. Role of Autophagy in cancer
6. Autophagy in tumor suppression
7. Autophagy in tumor promotion
8. Role of Autophagy in neurodegenerative diseases
9. Mechanism of autophagy in neurodegenerative disorders
10. Conclusion
11. References
12. Thank You
The document discusses various cancer treatment methods including surgery, radiotherapy, immunotherapy, hormone therapy, chemotherapy, and combination/adjuvant chemotherapy. It provides details on each method such as how surgery is used for diagnosis and removal of tumors, how different types of radiation are used in radiotherapy, and how chemotherapy works by destroying cancer cells. The document also covers natural compounds that can induce apoptosis in cancer cells, including plant extracts, flavonoids, and curcumin which suppresses prostaglandin formation through COX-2 inhibition. Nanoparticles are also discussed as a means of targeted drug delivery to cancer cells to reduce side effects.
Cancer is mainly caused by the conversion of proto-oncogenes into oncogenes. The process is known as oncogenesis.
This slide will help to get an idea about oncogenesis and also the proto-oncogenes which get converted.
Targeting Tumor Metabolism in Anti-Cancer Drug Discovery_Crimson PublishersCrimsonpublishersCancer
Cancer cells have evolved to develop sets of survival strategies to enable them not only to survive and ward off apoptosis-inducing effects of most chemotherapeutic drugs in current use but also proliferate and invade their surrounding healthy tissue. In the 1920’s, based on his pioneering research, Warburg hypothesized cancer cells rely on glycolysis for energy production to sustain their growth because their mitochondrial metabolism is dysfunctional. This review focuses on the current advances in cancer cell metabolism as a result of the recent resurgence of interests in the “Warburg hypothesis” (also called “Warburg effect”) and discusses how these advances have revealed potential anti-cancer drug targets. Additionally, we will also discuss metabolic pathways that are critically coupled to cancer cell survival and proliferation, thereby uncovering other putative anti-cancer drug targets for therapeutic consideration. Thus, we hope to provide a forward-looking framework for discussing and designing new anti-cancer therapies.
The document discusses various approaches to immunotherapy in cancers, including targeted therapies, biologic therapies, angiogenesis inhibitors, and immune-based therapies. It describes cellular processes like the cell cycle and cell kinetics that are relevant for cancer growth. It provides details on specific targeted therapies for pathways like EGFR, HER2/neu, VEGF, and PI3K/Akt/mTOR that are dysregulated in cancers. Immunotherapies like HPV vaccines have been successful in preventing cervical cancers associated with HPV infection. Overall, the document outlines current understandings and therapeutic approaches regarding tumor proliferation and immunotherapies for cancer.
1) The document discusses various barriers to targeting tumors including heterogeneity in blood flow within tumors and overexpression of efflux transporters in tumor cells.
2) It describes three main approaches to overcoming these barriers: passive targeting using the EPR effect, active targeting by attaching targeting ligands like antibodies, and physical targeting using stimuli like pH, temperature, or magnetic fields.
3) Examples are given of using each approach, such as pH-sensitive nanoparticles that degrade in the acidic tumor environment or magnetic drug targeting using nanoparticles guided by an external magnet.
GENOMICS 5
Use these Clues+Informatiom (Leacture) to help you type your paper.
Application of Genomics in Medicine
1. What is genomics?
Genomics is the study of genes of an organism, their compositions and the interaction amongst themselves and their environment.
2. What is the application of genomics in medicine?
This is the use of genetic material from a patient for the diagnosis of a disease or to decide which therapy is most suitable. Mostly used in oncology and detection of rare infectious diseases.
3.
4. How The application of genomics in medicine would benefit the world?
Improve the screening for cancers to ensure early diagnosis. If most of the cancers can be able to be detected early enough, they can be treated. Early detection can be aided by the use of genomics.
Genomics can help diagnose some genetically linked diseases. Some diseases are passed through genes. Understanding these diseases and defects can help tame them or treat them, and look for ways to avoid their occurrence in future generations.
Through genomics, drugs can be developed against various diseases. For instance, genomics on various disease causative agents can help a lot in identifying the most suitable drug against them.
Genomics can aide the storage of bioinformatics data, which is very essential. This data can be used even in premarital counseling where the couple can be advised on whether the combination of their genes could result in any genetic conditions to their expected babies. This can help reduce the cases of genetic disorders.
· of genomics in medicine
· Oral plant vaccines; these use DNA to create surface antigens when consumed. They show potential in the immunization against Hepatitis B. The research is still underway.
· Heterologous prime-boost vaccine for malaria; Ankara virus has been used to further develop two vaccines with DNA from P. falciparum. This has shown the prospects of reducing infection rates by 80%. This is expected to e used in future.
· Anti-malarial drugs; fosmidomycin is being tested for its effect on a component involved in the life cycle of the P. falciparum parasite, which could help in the treatment of malaria.
· Screening for thalassemias; PCR has been used to observe the mutations that lead to formation of hemoglobin. This has aided in genetic counseling which has seen a significant reduction in the cases of thalassemias.
· Precision medicine; this allows the doctors to prescribe treatment based on the patient’s genetic information. This is presently being used in the medical field.
· Pharmacogenomics; this involves testing the possible outcome when a patient takes a certain medicine. Through use of genomics it is possible to identify possible side effects. This is currently being applied in the medical field.
· Genome editing; this is the deleting or adding to some portions of gene sequenc ...
1. Gastric cancer is the fourth most common cancer worldwide and has a poor 5-year survival rate of less than 25%. It remains an active area of research.
2. Helicobacter pylori infection, which causes inflammation in the stomach, is a major risk factor for gastric cancer. Virulence factors in H. pylori can damage DNA and disrupt cell polarity pathways.
3. Loss of E-cadherin expression, which maintains cell adhesion and polarity, is also implicated in gastric carcinogenesis. E-cadherin mutations and methylation are associated with diffuse gastric cancer.
The central-dogma-oh-genetic-informationDaniel Madrid
The central dogma of genetics describes the flow of genetic information from DNA to RNA to proteins. Two articles discuss cancer-causing mechanisms related to this dogma. One found that the enzyme APOBEC3G can induce mutations during DNA replication that lead to cancer. The other identified that cancer cells rely on the protein SMARCAL1 to resolve replication stress and maintain telomere length through the ALT pathway. Further research is needed to identify targets of these carcinogenic processes to develop new treatment strategies.
Metabolomics is the large-scale study of small molecules, commonly known as metabolites, within cells, biofluids, tissues or organisms. Collectively, these small molecules and their interactions within a biological system are known as the metabolome.
Metabolomics is an analytical profiling technique for measuring and comparing large numbers of metabolites present in biological samples. Combining high-throughput analytical chemistry and multivariate data analysis, metabolomics offers a window on metabolic mechanisms.
The document discusses drug resistance in cancer therapy and antibiotic therapy. It provides causes and mechanisms of drug resistance, including alterations in drug targets, drug inactivation, reduced drug accumulation, and increased efflux pumps. Strategies to overcome resistance include pharmacokinetic monitoring, pharmacogenetic monitoring, and inhibiting efflux pumps. Drug resistance is a major challenge in cancer treatment and antibiotic use.
This document discusses controversies surrounding the use of cinnamon for managing diabetes. It reviews studies showing cinnamon has anti-inflammatory and antioxidant properties that could improve insulin resistance. However, human clinical trials have found varying results, with some showing no benefit and others finding improvements in factors like blood glucose, cholesterol, and blood pressure. While cinnamon may help lower fasting glucose levels, more research is still needed to determine its full effects and appropriate use for diabetes.
The document discusses the major challenges facing the drug industry, including making genomic discoveries into new therapeutics, increasing generic competition eroding revenue, and payers demanding evidence of economic benefits of new drugs. It then introduces a Nature Reprint Collection sponsored by Eli Lilly that provides analyses and perspectives on factors underlying challenges in drug innovation and potential scientific and strategic solutions. The collection includes articles on improving R&D productivity, network pharmacology, how new medicines are discovered, monoclonal antibody therapeutics, addressing variability in drug response, innovative R&D in China, impacts of mergers on R&D, crowd-sourcing in drug discovery, advancing clinical trial design, entrepreneurship in pharmaceutical R&D, and more.
Dieta hiperproteica para obeso com resistência à insulinaRuy Pantoja
This article discusses the potential benefits of low-carbohydrate diets for overweight patients with insulin resistance. It defines insulin resistance and its associated health risks like diabetes and cardiovascular disease. The article reviews studies that found individuals with insulin resistance tended to lose more weight and see greater reductions in insulin levels and other risk factors on low-carbohydrate diets compared to low-fat diets over short-term periods. It suggests low-carbohydrate diets may be particularly suitable for managing insulin resistance.
Ressecção parcial de pâncreas x regeneração x terapia incretínica humanosRuy Pantoja
Leahy et al. recently issued a consensus statement recommending targeting b-cell function early in therapy for type 2 diabetes. The consensus is based on evidence that declining b-cell function, a key pathogenesis of type 2 diabetes, begins early and drives disease progression. Preserving b-cell function may be possible through early intervention, even in lean type 2 diabetes patients. However, more research is needed to better understand b-cell dysfunction mechanisms involving both mass reduction and functional impairment over the natural course of diabetes. Non-invasive methods to measure b-cell mass longitudinally are also critical to evaluate early intervention effects and disease progression.
Brown adipose tissue, also known as brown fat, is a type of body fat that is able to burn calories to generate body heat. Unlike regular white fat, brown fat contains many small lipid droplets and a large number of mitochondria which give it a brownish color. The main function of brown fat is to generate heat by burning calories when a person is exposed to cold temperatures or takes cold showers.
This document reviews the potential for exploiting brown adipose tissue thermogenesis to treat obesity and diabetes. It discusses how increasing energy expenditure through cold exposure and activation of brown fat thermogenesis may induce less compensatory food intake than other methods, due to a "thermogenic disconnect". However, cold exposure also triggers other adaptive responses that can reduce energy expenditure. Overall, targeting thermogenic processes through brown fat activation seems a promising approach, but more research is needed to understand its effects and potential limitations.
1) Macrophages, immune cells that infiltrate tissues, play a crucial role in regulating body temperature through thermogenesis in brown fat tissue and by controlling the release of lipids from white fat tissue.
2) A study found that when mice were exposed to cold temperatures, their macrophages in brown and white fat tissues shifted to an anti-inflammatory form that is important for the thermogenic response. Disrupting genes related to this process impaired the mice's ability to generate and maintain body heat.
3) The findings suggest that the central nervous system relies on macrophages to mediate appropriate physiological responses to thermal demands, so studies manipulating macrophages may need re-evaluation, as effects could be due to changes in nervous system activity rather
This document discusses the role of 14-3-3 proteins in mediating the actions of insulin. It begins by explaining that insulin has wider physiological effects beyond regulating blood glucose levels, and that 14-3-3 proteins help integrate insulin signaling pathways. Specifically, 14-3-3 proteins bind to phosphorylated proteins regulated by the PI3K-PKB-mTORC1 and ERK-p90RSK pathways. They interact with AS160 and TBC1D1 to regulate glucose uptake in response to insulin and energy stress. Studying the dynamic 14-3-3 phosphoproteome is providing new insights into how insulin triggers shifts in metabolism.
Insulin is essential for regulating blood glucose levels. Type 1 and Type 2 diabetes result from insufficient insulin production or insulin resistance. Researchers are working to develop new therapies that target the molecular pathways involved in insulin production and secretion to restore normal blood glucose control in patients with diabetes.
Transfer RNA (tRNA) helps translate messenger RNA into proteins by carrying amino acids to the ribosome. Researchers have discovered that modifying tRNA through editing or altering its structure can influence the genetic code and protein synthesis. Precisely regulating tRNA may help treat diseases but also needs careful study to avoid unintended consequences.
Variant CDKAL1 is associated with type 2 diabetes. Two recent studies link CDKAL1 to the modification of a transfer RNA (tRNA) involved in protein translation. CDKAL1 adds a chemical group to tRNA that incorporates the amino acid lysine during protein synthesis. Mice deficient in CDKAL1 have reduced lysine in proinsulin, impairing its processing into insulin. This provides insight into how CDKAL1 variants may increase susceptibility to type 2 diabetes by disrupting insulin production.
1) DPP-IV is an enzyme that is increased in diabetes and cleaves proteins. The study found that DPP-IV cleaves HMGB1, an angiogenic protein involved in wound healing.
2) DPP-IV cleavage of HMGB1 inhibited its ability to induce endothelial cell migration and tube formation in vitro and vascular network formation in vivo.
3) The truncated form of HMGB1 was detected in diabetic patients, and treatment with DPP-IV inhibitors increased levels of full-length HMGB1. The study suggests DPP-IV inhibition may enhance HMGB1 activity and angiogenesis in diabetes.
This research article investigates how circulating glucose levels modulate neural control of the desire for high-calorie foods in humans. The study found that:
1) Mild hypoglycemia preferentially activated brain regions involved in reward and motivation (e.g. striatum, insula) and increased reported desire for high-calorie foods, compared to a state of euglycemia.
2) Euglycemia preferentially activated brain regions involved in inhibitory control (e.g. prefrontal cortex, anterior cingulate cortex) and resulted in less interest in food stimuli.
3) Higher circulating glucose levels predicted greater activation of the medial prefrontal cortex, and this response was absent in obese
Sitagliptina e proteção em ca diferenciado da tireóide.xRuy Pantoja
This document discusses whether anti-diabetic medications play a specific role in differentiated thyroid cancer compared to other cancer types. It reviews the prevalence of thyroid carcinoma in obese individuals, people with intermediate hyperglycemia, and diabetic patients compared to other cancers. It suggests that the over-expression of dipeptidyl peptidase IV (DPP-IV) in thyroid tumors, which is not seen in other cancer types, may be a potential reason for the unique relationship between thyroid cancer and diabetes.
This study examined the effects of ezetimibe treatment for 3 months on glucose metabolism in 96 Japanese patients with type 2 diabetes and hypercholesterolemia. Ezetimibe treatment significantly lowered LDL-cholesterol levels. HbA1c levels decreased in approximately 50% of patients after treatment. Univariate analysis found that changes in HbA1c were associated with serum alanine aminotransferase levels, aspartate aminotransferase to alanine aminotransferase ratio, and age. Higher baseline ALT levels and an AST/ALT ratio below 1.0 were significantly associated with decreases in HbA1c following ezetimibe administration, suggesting ezetimibe may improve glucose control through effects on
This document discusses inhibitors of dipeptidyl peptidase IV (DP IV) and aminopeptidase N (APN) and their potential role in treating acne. It finds:
1) DP IV and APN are expressed in human sebocytes, keratinocytes, and immune cells involved in acne pathogenesis.
2) Inhibitors of DP IV and APN suppressed sebocyte proliferation, enhanced differentiation, and increased anti-inflammatory cytokines in cell lines.
3) The inhibitors also suppressed immune cell proliferation and cytokine production ex vivo, suggesting anti-inflammatory effects.
4) Based on these findings, the study provides first evidence that DP IV and APN inhibitors
This document summarizes the similarities and differences between the two incretin hormones GIP and GLP-1. Both are secreted by the intestine in response to food intake and stimulate insulin secretion from pancreatic beta cells. They act through specific receptors and increase cyclic AMP levels. While they share this insulin-stimulating effect, they have different impacts on tissues like fat, bone, and brain. The document also discusses their secretion levels and metabolism, noting they are both degraded by DPP-4. It aims to provide an overview of these two important incretin hormones.
To my colleagues from many parts of the worldRuy Pantoja
Ruy Pantoja, a 62-year-old endocrinologist from Brazil, thanks colleagues from around the world for participating in an online forum to discuss metabolism. While he did not author any of the papers himself, he looks forward to receiving information from others on topics like BDNF, leptin, insulin, and glucagon and their interaction with the brain to control blood sugar. He finds it rewarding to upload scientific papers and see how many people download them. He will be in Lisbon for a conference and hopes some attendees can meet in person.
This letter discusses the safety of using the drug phentermine for long-term obesity treatment. It argues that contrary to common assumptions, phentermine does not typically elevate blood pressure and may even reduce it. The letter cites clinical trials and observational studies showing blood pressure declines in phentermine-treated patients, especially those with preexisting hypertension who lost weight. The authors conclude that long-term phentermine use is safer than assumed and should be the first-line pharmacotherapy considered for many obese patients. They call for additional long-term clinical trials of over 1 year to further evaluate phentermine's efficacy and safety profile.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
- 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
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics