New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes ...oscarandresparra
Researchers made two discoveries about proteins involved in DNA replication and prion diseases:
1) Scientists at UTMB found that the protein NEIL1 acts as a "cowcatcher" by scanning DNA for errors ahead of the replication machinery and signaling it to stop so repairs can be made. This revealed NEIL1's previously unknown role in replication error correction.
2) Researchers at Case Western modified a prion protein to stabilize its normal shape and prevent conversion to the abnormal form that causes diseases. Mice with this variant were resistant to prion infection, demonstrating this approach could block prion disease progression.
These studies provide new insights into DNA repair mechanisms and potential treatments for prion diseases.
P53 protein can repair DNA damage before cell replication. Studies found higher rates of germline DNA repair mutations in men with metastatic prostate cancer, such as with the BRCA1, BRCA2, MHSH2, and HOXB13 genes. These mutations were independent of family history and age of diagnosis. A limitation is that the studies only focused on specific genes and not how multiple genes may interact to influence disease. The student notes that identifying DNA mutations could help various cancer types and that education is needed on tobacco and UV radiation risks.
This document summarizes two scientific articles about DNA damage and repair mechanisms. The first article describes a discovery by University of Pennsylvania researchers about how DNA damage activates the immune system to target cancer cells. They propose using this knowledge to design new combination treatments. The second article discusses a new technique by University of North Carolina scientists to map DNA damage caused by cigarette smoking across the genome. This mapping revealed specific sites where repair was initiated following damage from cigarette carcinogens. Both advances could lead to improved cancer treatments and prevention strategies by deepening understanding of DNA replication and repair failures involved in disease.
The DNA is the most important part of the cell, as it contains all the information needed for cell maintenance, functioning, and life. Checkpoints in the cell cycle ensure this DNA is accurately replicated and passed to daughter cells. Failure of these mechanisms can lead to DNA damage and diseases like cancer. The document discusses DNA repair mechanisms like sister chromatid exchange and non-homologous end joining that help repair breaks, and how certain agents like radiation differently impact these processes. It also examines how polymorphisms in DNA repair genes may increase risk of diseases like cataracts by impacting the ability to repair UV damage.
Researchers at the UT Southwestern Medical Center and the University of Geneva studied how certain genes and proteins involved in maintaining genetic stability can sometimes contribute to cancer development. They found:
1) Mutations in the p53 tumor suppressor gene, which normally restrains mobile genetic elements, were prevalent in cancer samples. This leads to genomic instability by allowing increased movement of these elements within chromosomes.
2) The APOBEC protein, intended to fight viruses by modifying single-stranded DNA, can exploit weaknesses during human DNA replication to introduce mutations, as detected in tumor cells. It acts on the single strands present during replication fork separation.
3) Understanding how p53 and APOBEC influence genetic
The document summarizes two scientific articles from ScienceDaily about recent discoveries related to cell division and DNA replication that could provide new insights into cancer. The first article discusses a discovery of a protein complex called Ska that helps anchor DNA and distribute it correctly as cells divide. Understanding this complex could help develop new anti-cancer drugs. The second article describes an international study that improves ability to predict hereditary cancer risk by better classifying genetic variants associated with Lynch syndrome. This allows more accurate genetic counseling and preventive measures for at-risk families.
Eukaryotic cells have their genetic material in the nucleus, in the other side, prokaryotes have it dispersed in the cytoplasm.
From this DNA will be synthesized RNA, which will act as an intermediary, carrying genetic information from the nucleus to the ribosomes located in the cytoplasm to carry out protein synthesis.
genetic code consists of 64 triplets (codons) of nucleotides, each codon encodes for one of the 20 amino-acids used in the synthesis of proteins.
The study of the genetic code, allow s us identify mutations in specific genes, to detect diseases or predispositions to some pathologies such as those proposed by the articles, and with tan information, implement a PREVENTIVE MEDICINE.
Knowing the sequence of genes that cause certain genetic diseases, is essential for GENE THERAPY branch. In brief it consist in introduce a correct copy of the defective gene that was visualized into the cells, by some vectors, previously studied.
With the knowledge of genetic information, can be provided counseling before and after pregnancy to future parents (Give information about the diseases to which it is susceptible and existing treatments), having always instilled an ethical principle: THE HUMAN LIFE RESPECT.
Promote investigation in medicine basic areas, such as cell biology, molecular biology, biochemistry and pharmacology, with the aim of implement humanity solutions .
New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes ...oscarandresparra
Researchers made two discoveries about proteins involved in DNA replication and prion diseases:
1) Scientists at UTMB found that the protein NEIL1 acts as a "cowcatcher" by scanning DNA for errors ahead of the replication machinery and signaling it to stop so repairs can be made. This revealed NEIL1's previously unknown role in replication error correction.
2) Researchers at Case Western modified a prion protein to stabilize its normal shape and prevent conversion to the abnormal form that causes diseases. Mice with this variant were resistant to prion infection, demonstrating this approach could block prion disease progression.
These studies provide new insights into DNA repair mechanisms and potential treatments for prion diseases.
P53 protein can repair DNA damage before cell replication. Studies found higher rates of germline DNA repair mutations in men with metastatic prostate cancer, such as with the BRCA1, BRCA2, MHSH2, and HOXB13 genes. These mutations were independent of family history and age of diagnosis. A limitation is that the studies only focused on specific genes and not how multiple genes may interact to influence disease. The student notes that identifying DNA mutations could help various cancer types and that education is needed on tobacco and UV radiation risks.
This document summarizes two scientific articles about DNA damage and repair mechanisms. The first article describes a discovery by University of Pennsylvania researchers about how DNA damage activates the immune system to target cancer cells. They propose using this knowledge to design new combination treatments. The second article discusses a new technique by University of North Carolina scientists to map DNA damage caused by cigarette smoking across the genome. This mapping revealed specific sites where repair was initiated following damage from cigarette carcinogens. Both advances could lead to improved cancer treatments and prevention strategies by deepening understanding of DNA replication and repair failures involved in disease.
The DNA is the most important part of the cell, as it contains all the information needed for cell maintenance, functioning, and life. Checkpoints in the cell cycle ensure this DNA is accurately replicated and passed to daughter cells. Failure of these mechanisms can lead to DNA damage and diseases like cancer. The document discusses DNA repair mechanisms like sister chromatid exchange and non-homologous end joining that help repair breaks, and how certain agents like radiation differently impact these processes. It also examines how polymorphisms in DNA repair genes may increase risk of diseases like cataracts by impacting the ability to repair UV damage.
Researchers at the UT Southwestern Medical Center and the University of Geneva studied how certain genes and proteins involved in maintaining genetic stability can sometimes contribute to cancer development. They found:
1) Mutations in the p53 tumor suppressor gene, which normally restrains mobile genetic elements, were prevalent in cancer samples. This leads to genomic instability by allowing increased movement of these elements within chromosomes.
2) The APOBEC protein, intended to fight viruses by modifying single-stranded DNA, can exploit weaknesses during human DNA replication to introduce mutations, as detected in tumor cells. It acts on the single strands present during replication fork separation.
3) Understanding how p53 and APOBEC influence genetic
The document summarizes two scientific articles from ScienceDaily about recent discoveries related to cell division and DNA replication that could provide new insights into cancer. The first article discusses a discovery of a protein complex called Ska that helps anchor DNA and distribute it correctly as cells divide. Understanding this complex could help develop new anti-cancer drugs. The second article describes an international study that improves ability to predict hereditary cancer risk by better classifying genetic variants associated with Lynch syndrome. This allows more accurate genetic counseling and preventive measures for at-risk families.
Eukaryotic cells have their genetic material in the nucleus, in the other side, prokaryotes have it dispersed in the cytoplasm.
From this DNA will be synthesized RNA, which will act as an intermediary, carrying genetic information from the nucleus to the ribosomes located in the cytoplasm to carry out protein synthesis.
genetic code consists of 64 triplets (codons) of nucleotides, each codon encodes for one of the 20 amino-acids used in the synthesis of proteins.
The study of the genetic code, allow s us identify mutations in specific genes, to detect diseases or predispositions to some pathologies such as those proposed by the articles, and with tan information, implement a PREVENTIVE MEDICINE.
Knowing the sequence of genes that cause certain genetic diseases, is essential for GENE THERAPY branch. In brief it consist in introduce a correct copy of the defective gene that was visualized into the cells, by some vectors, previously studied.
With the knowledge of genetic information, can be provided counseling before and after pregnancy to future parents (Give information about the diseases to which it is susceptible and existing treatments), having always instilled an ethical principle: THE HUMAN LIFE RESPECT.
Promote investigation in medicine basic areas, such as cell biology, molecular biology, biochemistry and pharmacology, with the aim of implement humanity solutions .
1. Researchers have discovered a new four-stranded quadruple helix DNA structure called G-quadruplexes that exists in human genomes, particularly in regions rich in guanine. These quadruplexes are more common in rapidly dividing cells like cancer cells.
2. A separate study identified new sites in cells where DNA breaks early in the replication process. These break sites correlate with damage seen in cancers like diffuse large B cell lymphoma. Comparing mouse and human cells, both exhibit similar trends of genome instability at these sites.
3. Discoveries of DNA structures and break sites help understand the origins of diseases and cancer, offering new treatment approaches through stopping replication in cancer cells or addressing instability.
DNA structure, genes and its chemical compositionValentina Duque
The document discusses the importance of understanding DNA structure and genes. It notes that DNA contains the genetic material of organisms and understanding a person's DNA can help identify genetic mutations that may cause diseases. This allows for focused treatment and prevention strategies. The document also discusses two recent studies: one discovered a new gene variant present in 3% of ALS cases, and the other found genetic variants linked to academic achievement that can help identify children at risk for learning difficulties. Understanding DNA structure is thus essential for medicine and treatment.
The document discusses two scientific discoveries. The first is that an enzyme called UvrD was found to reverse stalled transcription machinery in E. coli, allowing RNA polymerase to backtrack and expose problems in the DNA strand to facilitate repair without terminating transcription. The second discovery found that a genetic mutation in the DNA repair gene POLB in mice unexpectedly caused lupus-like symptoms, identifying a potential genetic cause of the autoimmune disease lupus in humans. Finding the causes of diseases like lupus could help develop new and less toxic treatments. Both discoveries provide insights that could improve understanding of diseases and lead to better prevention and treatment options.
This individual has over 15 years of experience in biochemistry and cancer research. Their postdoctoral research identified a compound that is currently in preclinical trials for cancer. They currently hold adjunct faculty positions teaching biology and have mentored master's students. Their research focuses on developing cancer therapeutics by identifying inhibitors of DNA repair enzymes.
1) Researchers at Penn State used stem cells and a modified Wnt signaling pathway to generate epicardium and endocardium cells, which could help regenerate the layers of the human heart and improve quality of life for heart attack patients.
2) A rare and severe form of encephalitis called anti-NMDA receptor encephalitis attacks NMDA receptors in the brain; a new treatment using the drug Bortezomib was found to successfully reduce antibodies and symptoms by inhibiting proteasomes.
3) Advances in regenerating heart cells and treating difficult diseases bring hope and move humanity forward as medical solutions are found for problems that were previously intractable.
Geneticists from the USA and Japan used iPSC to replace ring chromosomes, which cause short stature and mental retardation, with normal chromosomes in cell cultures from 5 patients. The therapy was successful in replacing ring chromosomes from chromosomes 13 and 18, but not other defects. Additionally, a study found variations in non-coding DNA, not just known risks like age and weight, increase risk of type 2 diabetes. Over 300 million people worldwide have diabetes, so further study of non-coding DNA could help understand disease development and identify new treatment approaches. Both studies provide potential ways to address genetic defects and help patients through stem cell therapy or risk assessment.
This document summarizes the research of Jon Cooper's lab on various forms of Batten disease. The lab is moving from London to Los Angeles to further its research. The lab studies how protein and DNA mutations lead to Batten disease and aims to determine where in the body and brain pathology occurs. Research suggests pathology begins early in the spinal cord and peripheral nervous system before affecting the brain. The lab grows brain cells from mice models of different forms of Batten disease to study how nerve and glial cells are differently affected and how this impacts disease progression and symptoms. Understanding these disease mechanisms could help identify new treatment approaches.
This document presents two cases of juvenile onset neuronal ceroid lipofuscinosis (NCL) caused by compound heterozygous missense mutations in the CTSD gene. Case 1 is a 13-year-old male who began experiencing developmental issues at age 6 and vision loss at age 6. Case 2 is a 19-year-old male who had mild delays and vision loss beginning at age 5. Both experienced progressive neurological and cognitive decline. These cases demonstrate phenotypic variability is possible even from the same gene mutations, and help characterize the range of presentation of CTSD-related NCL beyond the classic severe congenital form.
This document provides a summary of recommended readings in neuro-oncology for 2012. It lists several journal articles covering topics such as the genetic underpinnings of gliomas, surgical and radiotherapy techniques for brain tumors, treatments for brain metastases, high-grade and low-grade gliomas, primary CNS lymphomas, and palliative care in neuro-oncology. The articles examine factors like mutations in IDH1, H3F3A, and other genes; surgical resection outcomes; chemotherapy responses; and quality of life for brain tumor patients.
The document summarizes two scientific articles about recent advances in molecular biology research. The first article describes how researchers reconstituted the DNA replication fork, the structure where new DNA strands are synthesized, for the first time using yeast cell enzymes. This allows them to study the replication process and regulation in fine detail. The second article discusses the discovery of an enzyme involved in metabolism located in the cell nucleus, rather than the mitochondria as expected. This finding links metabolism to DNA regulation and could help understand common diseases. The student observes that this research provides opportunities to improve health and lives by advancing understanding of genetic information and disease processes.
Biology and medicine have a close relationship where biology serves as an important tool for medicine. Studies on cellular metabolism and the role of proteins in cell division have helped further our understanding of diseases from the beginning. Research on a single protein that controls genetic networks essential for sperm development found that without this protein, sperm development is abnormal. A separate study on mitochondrial diseases found they are becoming more frequent and costly to healthcare systems, highlighting the need for improved prevention and treatment strategies. Advances in understanding basic biological mechanisms allow for more effective diagnosis and management of illnesses.
This document summarizes two scientific studies on chromosome defects and genetic diseases. The first study discovered a chromosome therapy technique to correct severe chromosome defects by replacing an abnormal ring chromosome with a normal duplicated chromosome in stem cells. This could help repair birth defects. The second study found that analyzing chromatin architecture, the organization of DNA and proteins in chromosomes, could help identify regulatory DNA anomalies and better diagnose genetic diseases, since DNA sequencing alone is insufficient. This discovery paves the way for improved understanding and diagnosis of many genetic conditions.
2014 education course cell therapy in ocular disease-description-and-agenda-2...John Redaelli
This document provides an agenda for a conference on "Cell Therapy in Ocular Disease — Emerging Research and Therapy" being held on May 3, 2014 in Orlando, Florida. The conference will review current approaches to cell therapy for both corneal and retinal conditions, with a focus on translating basic research into human therapies. Speakers will discuss emerging research areas and cell therapies currently in clinical trials. Participants will gain an understanding of the state of clinical/translational therapies, challenges of translation, and unmet needs in cell therapy. The agenda lists talks on topics such as corneal stem cell therapy, retinal progenitor cells for retinitis pigmentosa treatment, transplantation of embryonic stem cell-derived retinal pigment epithelium, and mechanisms for long
This study tested intrathecal enzyme replacement therapy (ERT) in a mouse model of infantile Batten disease. Mice lacking the enzyme palmitoyl-protein thioesterase 1 (PPT1) received a single intrathecal injection of recombinant human PPT1 at 6 weeks of age. This prevented decline in motor function, improved survival, and reduced brain and spinal cord pathology compared to untreated mice. The effects were similar to ERT for another form of Batten disease. This suggests intrathecal ERT may help treat infantile Batten disease caused by PPT1 deficiency in humans.
A gene therapy targeting the eye may help treat vision loss in juvenile Batten disease patients by slowing or stopping the progression of retinal degeneration. The retina contains light-sensitive cells that are essential for vision but are lost in juvenile Batten disease due to a genetic defect. While other therapies aim to treat symptoms in the brain, the eye has not been targeted yet. Gene therapy could introduce healthy copies of the defective gene into photoreceptor cells via a virus delivered by subretinal injection to improve vision and quality of life for patients.
The document discusses several studies related to DNA and cancer. A study identified a gene, NFIB, that is overexpressed in mouse and human lung tumors and appears to drive progression of small cell lung cancer. Another study revealed the molecular mechanism that promotes cancer development by characterizing regions of DNA that are more susceptible to breakage in early cancer development. A third study identified the molecular basis for DNA breakage in cancer cells.
The Batten Animal Research Network (BARN) is an international collaboration between research groups studying animal models of Batten disease. The groups share resources like cell cultures and animal models, exchange students, visit each other, and plan research together. BARN has developed measures of disease progression in sheep models to test potential drug and gene therapies. Recent work includes developing neuronal cultures from sheep models to study early disease stages, identifying mutations that cause two forms of CLN6 disease and CLN5 disease, and analyzing the neuroinflammatory response over time. Gene therapy trials using AAV vectors are underway in CLN5 and CLN6 sheep models.
Wood smoke and polycyclic aromatic hydrocarbons can cause direct DNA damage through free radicals and lipid peroxidation. There are several types of DNA damage including damage from ultraviolet light, deamination, and depurination. The cell has multiple pathways to repair damaged DNA, including direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Defects in DNA repair pathways can cause genetic diseases like xeroderma pigmentosum and Cockayne syndrome. Xeroderma pigmentosum patients are highly susceptible to skin cancers due to an inability to repair UV damage.
DNA repair is a collection of processes cells use to identify and correct damage to DNA. Failure to repair damaged DNA leads to mutations, which are permanent changes in the DNA sequence. There are several types of DNA damage including mismatches, modified DNA bases, and single or double strand breaks. Cells use multiple repair pathways like direct reversal, base excision repair, nucleotide excision repair, recombination repair, and translesion DNA synthesis to fix different types of DNA damage. Homologous recombination repairs double strand breaks by exchanging DNA between similar molecules, while site-specific and transposon recombination involve movement of DNA between defined sequences.
1. Researchers have discovered a new four-stranded quadruple helix DNA structure called G-quadruplexes that exists in human genomes, particularly in regions rich in guanine. These quadruplexes are more common in rapidly dividing cells like cancer cells.
2. A separate study identified new sites in cells where DNA breaks early in the replication process. These break sites correlate with damage seen in cancers like diffuse large B cell lymphoma. Comparing mouse and human cells, both exhibit similar trends of genome instability at these sites.
3. Discoveries of DNA structures and break sites help understand the origins of diseases and cancer, offering new treatment approaches through stopping replication in cancer cells or addressing instability.
DNA structure, genes and its chemical compositionValentina Duque
The document discusses the importance of understanding DNA structure and genes. It notes that DNA contains the genetic material of organisms and understanding a person's DNA can help identify genetic mutations that may cause diseases. This allows for focused treatment and prevention strategies. The document also discusses two recent studies: one discovered a new gene variant present in 3% of ALS cases, and the other found genetic variants linked to academic achievement that can help identify children at risk for learning difficulties. Understanding DNA structure is thus essential for medicine and treatment.
The document discusses two scientific discoveries. The first is that an enzyme called UvrD was found to reverse stalled transcription machinery in E. coli, allowing RNA polymerase to backtrack and expose problems in the DNA strand to facilitate repair without terminating transcription. The second discovery found that a genetic mutation in the DNA repair gene POLB in mice unexpectedly caused lupus-like symptoms, identifying a potential genetic cause of the autoimmune disease lupus in humans. Finding the causes of diseases like lupus could help develop new and less toxic treatments. Both discoveries provide insights that could improve understanding of diseases and lead to better prevention and treatment options.
This individual has over 15 years of experience in biochemistry and cancer research. Their postdoctoral research identified a compound that is currently in preclinical trials for cancer. They currently hold adjunct faculty positions teaching biology and have mentored master's students. Their research focuses on developing cancer therapeutics by identifying inhibitors of DNA repair enzymes.
1) Researchers at Penn State used stem cells and a modified Wnt signaling pathway to generate epicardium and endocardium cells, which could help regenerate the layers of the human heart and improve quality of life for heart attack patients.
2) A rare and severe form of encephalitis called anti-NMDA receptor encephalitis attacks NMDA receptors in the brain; a new treatment using the drug Bortezomib was found to successfully reduce antibodies and symptoms by inhibiting proteasomes.
3) Advances in regenerating heart cells and treating difficult diseases bring hope and move humanity forward as medical solutions are found for problems that were previously intractable.
Geneticists from the USA and Japan used iPSC to replace ring chromosomes, which cause short stature and mental retardation, with normal chromosomes in cell cultures from 5 patients. The therapy was successful in replacing ring chromosomes from chromosomes 13 and 18, but not other defects. Additionally, a study found variations in non-coding DNA, not just known risks like age and weight, increase risk of type 2 diabetes. Over 300 million people worldwide have diabetes, so further study of non-coding DNA could help understand disease development and identify new treatment approaches. Both studies provide potential ways to address genetic defects and help patients through stem cell therapy or risk assessment.
This document summarizes the research of Jon Cooper's lab on various forms of Batten disease. The lab is moving from London to Los Angeles to further its research. The lab studies how protein and DNA mutations lead to Batten disease and aims to determine where in the body and brain pathology occurs. Research suggests pathology begins early in the spinal cord and peripheral nervous system before affecting the brain. The lab grows brain cells from mice models of different forms of Batten disease to study how nerve and glial cells are differently affected and how this impacts disease progression and symptoms. Understanding these disease mechanisms could help identify new treatment approaches.
This document presents two cases of juvenile onset neuronal ceroid lipofuscinosis (NCL) caused by compound heterozygous missense mutations in the CTSD gene. Case 1 is a 13-year-old male who began experiencing developmental issues at age 6 and vision loss at age 6. Case 2 is a 19-year-old male who had mild delays and vision loss beginning at age 5. Both experienced progressive neurological and cognitive decline. These cases demonstrate phenotypic variability is possible even from the same gene mutations, and help characterize the range of presentation of CTSD-related NCL beyond the classic severe congenital form.
This document provides a summary of recommended readings in neuro-oncology for 2012. It lists several journal articles covering topics such as the genetic underpinnings of gliomas, surgical and radiotherapy techniques for brain tumors, treatments for brain metastases, high-grade and low-grade gliomas, primary CNS lymphomas, and palliative care in neuro-oncology. The articles examine factors like mutations in IDH1, H3F3A, and other genes; surgical resection outcomes; chemotherapy responses; and quality of life for brain tumor patients.
The document summarizes two scientific articles about recent advances in molecular biology research. The first article describes how researchers reconstituted the DNA replication fork, the structure where new DNA strands are synthesized, for the first time using yeast cell enzymes. This allows them to study the replication process and regulation in fine detail. The second article discusses the discovery of an enzyme involved in metabolism located in the cell nucleus, rather than the mitochondria as expected. This finding links metabolism to DNA regulation and could help understand common diseases. The student observes that this research provides opportunities to improve health and lives by advancing understanding of genetic information and disease processes.
Biology and medicine have a close relationship where biology serves as an important tool for medicine. Studies on cellular metabolism and the role of proteins in cell division have helped further our understanding of diseases from the beginning. Research on a single protein that controls genetic networks essential for sperm development found that without this protein, sperm development is abnormal. A separate study on mitochondrial diseases found they are becoming more frequent and costly to healthcare systems, highlighting the need for improved prevention and treatment strategies. Advances in understanding basic biological mechanisms allow for more effective diagnosis and management of illnesses.
This document summarizes two scientific studies on chromosome defects and genetic diseases. The first study discovered a chromosome therapy technique to correct severe chromosome defects by replacing an abnormal ring chromosome with a normal duplicated chromosome in stem cells. This could help repair birth defects. The second study found that analyzing chromatin architecture, the organization of DNA and proteins in chromosomes, could help identify regulatory DNA anomalies and better diagnose genetic diseases, since DNA sequencing alone is insufficient. This discovery paves the way for improved understanding and diagnosis of many genetic conditions.
2014 education course cell therapy in ocular disease-description-and-agenda-2...John Redaelli
This document provides an agenda for a conference on "Cell Therapy in Ocular Disease — Emerging Research and Therapy" being held on May 3, 2014 in Orlando, Florida. The conference will review current approaches to cell therapy for both corneal and retinal conditions, with a focus on translating basic research into human therapies. Speakers will discuss emerging research areas and cell therapies currently in clinical trials. Participants will gain an understanding of the state of clinical/translational therapies, challenges of translation, and unmet needs in cell therapy. The agenda lists talks on topics such as corneal stem cell therapy, retinal progenitor cells for retinitis pigmentosa treatment, transplantation of embryonic stem cell-derived retinal pigment epithelium, and mechanisms for long
This study tested intrathecal enzyme replacement therapy (ERT) in a mouse model of infantile Batten disease. Mice lacking the enzyme palmitoyl-protein thioesterase 1 (PPT1) received a single intrathecal injection of recombinant human PPT1 at 6 weeks of age. This prevented decline in motor function, improved survival, and reduced brain and spinal cord pathology compared to untreated mice. The effects were similar to ERT for another form of Batten disease. This suggests intrathecal ERT may help treat infantile Batten disease caused by PPT1 deficiency in humans.
A gene therapy targeting the eye may help treat vision loss in juvenile Batten disease patients by slowing or stopping the progression of retinal degeneration. The retina contains light-sensitive cells that are essential for vision but are lost in juvenile Batten disease due to a genetic defect. While other therapies aim to treat symptoms in the brain, the eye has not been targeted yet. Gene therapy could introduce healthy copies of the defective gene into photoreceptor cells via a virus delivered by subretinal injection to improve vision and quality of life for patients.
The document discusses several studies related to DNA and cancer. A study identified a gene, NFIB, that is overexpressed in mouse and human lung tumors and appears to drive progression of small cell lung cancer. Another study revealed the molecular mechanism that promotes cancer development by characterizing regions of DNA that are more susceptible to breakage in early cancer development. A third study identified the molecular basis for DNA breakage in cancer cells.
The Batten Animal Research Network (BARN) is an international collaboration between research groups studying animal models of Batten disease. The groups share resources like cell cultures and animal models, exchange students, visit each other, and plan research together. BARN has developed measures of disease progression in sheep models to test potential drug and gene therapies. Recent work includes developing neuronal cultures from sheep models to study early disease stages, identifying mutations that cause two forms of CLN6 disease and CLN5 disease, and analyzing the neuroinflammatory response over time. Gene therapy trials using AAV vectors are underway in CLN5 and CLN6 sheep models.
Wood smoke and polycyclic aromatic hydrocarbons can cause direct DNA damage through free radicals and lipid peroxidation. There are several types of DNA damage including damage from ultraviolet light, deamination, and depurination. The cell has multiple pathways to repair damaged DNA, including direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Defects in DNA repair pathways can cause genetic diseases like xeroderma pigmentosum and Cockayne syndrome. Xeroderma pigmentosum patients are highly susceptible to skin cancers due to an inability to repair UV damage.
DNA repair is a collection of processes cells use to identify and correct damage to DNA. Failure to repair damaged DNA leads to mutations, which are permanent changes in the DNA sequence. There are several types of DNA damage including mismatches, modified DNA bases, and single or double strand breaks. Cells use multiple repair pathways like direct reversal, base excision repair, nucleotide excision repair, recombination repair, and translesion DNA synthesis to fix different types of DNA damage. Homologous recombination repairs double strand breaks by exchanging DNA between similar molecules, while site-specific and transposon recombination involve movement of DNA between defined sequences.
DNA repair mechanisms are essential for maintaining genomic integrity. There are several pathways for repairing different types of DNA damage: mismatch repair fixes errors during DNA replication, base excision repair removes damaged bases, nucleotide excision repair replaces larger sections of damaged DNA, and double-strand break repair fixes breaks in both DNA strands. Defects in DNA repair genes can lead to increased cancer risks and genetic disorders like xeroderma pigmentosum and Fanconi anemia. Overall, DNA repair helps prevent mutations from being passed to new cells.
This document discusses DNA repair mechanisms. It begins with an introduction to DNA damage and sources of damage like base modifications, replication errors, and radiation. It then covers the major DNA repair pathways: direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Double strand break repair can occur through direct joining or homologous recombination. DNA damage checkpoints pause the cell cycle to allow for repair. Defects in repair pathways cause hereditary disorders like xeroderma pigmentosum and Werner syndrome.
Genetic stability relies on accurate DNA replication and repair mechanisms to correct approximately 1 million lesions per cell per day caused by various sources of DNA damage. If unrepaired, this damage can lead to mutations, genetic diseases like cancer, or cell death. The cell has multiple pathways to repair DNA damage, including base excision repair, nucleotide excision repair, mismatch repair, and homologous recombination. Homologous recombination is especially important for repairing double-stranded breaks using the undamaged sister chromatid as a template, and involves proteins such as RAD51, BRCA1, BRCA2, ATM, and the Fanconi anemia/BRCA pathway. Defects in DNA repair genes are
The document discusses various types of DNA damage including deamination, depurination, UV light-induced T-T and T-C dimers, alkylation, oxidative damage, replication errors, and double-strand breaks. It then summarizes different DNA repair pathways such as base excision repair, nucleotide excision repair, mismatch repair, direct repair, recombination repair, and non-homologous end-joining. The SOS response in bacteria is also summarized as activating error-prone repair when normal repair pathways are overwhelmed.
1. DNA repair is a collection of processes by which cells identify and correct damage to DNA molecules to maintain the integrity of the genome.
2. There are several pathways of DNA repair including base excision repair, nucleotide excision repair, mismatch repair, non-homologous end joining, and homologous recombination.
3. Defects in DNA repair pathways can lead to increased mutations, cancer, and cell death if damage is left unrepaired.
1) DNA mutations can occur spontaneously from errors in replication or due to environmental mutagens, and can lead to genetic disorders if unrepaired.
2) The cell has multiple DNA repair mechanisms to recognize and fix damage, such as base excision repair and nucleotide excision repair. Failure to repair can increase mutations.
3) The study found that DNA damage increased phosphorylation and nuclear localization of the tumor suppressor PTEN, which plays a role in DNA repair and maintaining genomic integrity. Phosphorylation of PTEN was associated with enhanced DNA repair.
1. Mutations can occur through errors in DNA replication, repair, or recombination which can cause substitutions, insertions or deletions of DNA bases. Environmental mutagens like radiation and chemicals can also directly interact with DNA and cause mutations.
2. Some mutations involve changes to a single DNA base pair, while others are larger scale mutations affecting longer DNA segments. Point mutations may substitute one base for another, while insertions or deletions can disrupt the DNA reading frame.
3. Cells have mechanisms like direct repair and photoreactivation to correct some mutations, but errors in these pathways can also lead to mutations if not repaired properly.
DNA repair mechanisms are developed by cells to repair various types of DNA damage induced by chemicals, radiation, and other factors. These repair mechanisms include base excision repair, nucleotide excision repair, strand break repair, and mismatch repair. Recent studies have found new enzymes and gene switches that may play an important role in DNA repair and preventing cancer by contributing to accurate chromosome segregation and reducing genome instability. Understanding DNA repair pathways could provide opportunities to develop new cancer therapies by preventing initial DNA damage or enhancing the body's natural repair processes.
DNA repair mechanisms identify and correct damage to DNA that occurs due to normal cellular processes and environmental factors. There are two main types of DNA damage: endogenous damage caused by normal cellular processes and exogenous damage caused by external agents like UV radiation and chemicals. The main repair mechanisms are base excision repair, nucleotide excision repair, direct repair via photolyases, and error-prone repair systems like SOS repair. Together, these pathways maintain genome integrity by repairing different types of DNA lesions.
This document discusses DNA repair mechanisms and two related studies. It first provides an introduction to how cells use DNA repair mechanisms to detect and correct damage to prevent mutations. It then summarizes two studies: one identifying the FAN1 gene which may be involved in repairing DNA damage in the Fanconi anemia pathway, and another finding that the drug Olaparib, which inhibits the DNA repair enzyme PARP, caused tumors to shrink in women with BRCA gene mutations and breast or ovarian cancer. It concludes by discussing the potential medical applications of further understanding DNA repair mechanisms and using drugs like Olaparib to treat cancer.
This document discusses gene mutation and DNA repair. It defines mutation as a heritable change in genetic material, which can be caused by spontaneous or induced events. Spontaneous mutations arise from errors in DNA replication, while induced mutations are caused by environmental mutagens. The main types of mutations are point mutations, insertions, deletions, and chromosomal rearrangements. Mutations can occur in germ-line or somatic cells and affect the genotype and phenotype in various ways. Organisms have developed DNA repair mechanisms to correct mutations but some mutations still occur.
The document provides an overview of DNA repair, including:
1) DNA is the only biological macromolecule that is repaired, as spontaneous and environmentally-induced damage occurs daily.
2) There are multiple pathways of DNA repair, including direct reversal, base excision repair, nucleotide excision repair, and double-strand break repair.
3) Defects in DNA repair can lead to genetic disorders and cancer, highlighting the importance of effective repair.
The document discusses bioenergetics and ATP production. It covers:
1. Cell structure including the cell membrane, nucleus, and mitochondria.
2. ATP is the energy currency of cells and is produced through anaerobic and aerobic pathways.
3. Anaerobic pathways include phosphocreatine breakdown and glycolysis, which produces ATP without oxygen. Aerobic pathways use oxygen during oxidative phosphorylation to produce ATP.
4. Glycolysis breaks down glucose to pyruvate or lactate, producing ATP. The NADH and FADH2 produced carry electrons to fuel aerobic ATP production.
Biología del Cáncer Robert Weinberg presentacion capitulos 12 - 16Ivan Falconi
Este documento describe los mecanismos de reparación del ADN y los factores que pueden dañar el ADN y provocar mutaciones y posiblemente cáncer. Explica que el ADN está sujeto a daños espontáneos o inducidos y que las células tienen varios mecanismos como BER, NER y MMR para reparar errores. También describe varios agentes mutágenos endógenos como especies reactivas de oxígeno y factores exógenos como UV, agentes alquilantes y toxinas que pueden dañ
This document summarizes several DNA repair mechanisms: mismatch repair removes errors that escape proofreading; base excision repair uses a base-flipping mechanism to remove damaged bases; nucleotide excision repair cleaves damaged DNA on either side of a lesion. It also discusses transcription coupled repair helping RNA polymerase past lesions, double strand break repair using homologous recombination, and photo reactivation using light energy to repair DNA. The document was authored by BHARATESHA.S for their 7th semester molecular biology course guided by CHANDRAKANTH.R.
This document discusses two scientific articles about cellular processes and potential applications to cancer treatment. The first article describes how a newly identified protease, Wss1, can chop down the protein components of DNA-protein crosslinks, allowing cells to replicate their genome. The second article discusses how DNA origami was used to test the effects of ephrin placement on the EphA2 receptor in cancer cells, finding it reduced invasiveness. The document concludes that further research using specialized techniques can improve understanding of disease pathophysiology and lead to potential cures in the future.
DNA is a long polymer of simple units called nucleotides. Each one contains a phosphate group (acid component), a sugar group (neutral component) and a nitrogen base (basic component).
This document summarizes and reviews two medical news articles about recent research on DNA damage and repair. The first study found that cancer cells may simplify their genomes to proliferate more easily, making the cells more vulnerable to DNA-damaging drugs. The second mapped the specific locations in the genome where cigarette smoking causes DNA damage, providing insights to help prevent and treat smoking-related lung cancer. The student concludes that further investigating DNA repair and damage mechanisms could reveal new treatment strategies and advance the understanding and prevention of diseases like cancer.
Scientists have discovered new details of the biochemical interactions necessary for cell division. They captured images of the helicase enzyme that unwinds DNA as it gets drawn to and wraps around its target. Additionally, BCM scientists unraveled the mystery behind spontaneous DNA breaks in resting cells not undergoing replication. They determined that "R loops" consisting of hybrid RNA-DNA structures can produce double-strand breaks, explaining how DNA fragmentation can occur without external intervention. The findings provide a better understanding of essential biological processes like DNA replication and could enable new ways to fight cancer by controlling when cells divide.
A group of Swedish and Russian scientists led by Sergey Nikolaev argue that the APOBEC protein, which normally protects against viruses, takes advantage of DNA replication weaknesses to insert mutations into the genome. The APOBEC protein acts when the lagging strand is single-stranded, causing early mutations in important genes. Studying yeast cells provided new insights into how replication can go wrong and when. Understanding DNA replication could help intervene in copying errors to ensure proper genome replication and improve patient quality of life. Further research on proteins influencing replication errors may help prevent cancers.
The document discusses recent discoveries about cell division and chromosomes that could help understand disorders like cancer. Researchers discovered the Ska complex of proteins that stabilize cell division by anchoring DNA to cell strands during division. Mistakes in this process can cause cancer. Scientists also used normal chromosomes to replace defective ring chromosomes in skin cells, correcting genetic disorders. Understanding these processes may enable new treatments for cancer and genetic disorders by controlling cell division and repairing chromosome defects.
The document summarizes several studies on DNA replication and the molecular machinery involved. It describes how researchers used tools like molecular biology and biochemistry to slow down and "freeze" the replication process at intermediate steps. This allowed them to observe conformational changes in proteins like the origin recognition complex (ORC) as it recruits the helicase enzyme to unwind DNA. Cryo-electron microscopy was then used to capture 3D structures of the protein components and reveal how they interact during replication initiation. The studies provide new insights into this critical cellular process.
The mechanisms of DNA repair help us maintain the body in a normal physiological state, despite of the constant inducing damage that we are exposed.
But if these repair mechanisms fail for some reason it could cause mutations, cell death and many diseases.
Therefore, a low mutation rate indicates the efficiency of repair mechanisms, but a failure of these will be the cause of several mutations.
Several studies point to the discovery of new mechanisms of repair, so try to create treatments for diseases.
The document discusses two studies related to DNA methylation. The first study found that cancer incidence increases with age due to age-related methylation across the human genome, which can negatively impact gene expression and increase cancer risk. The second study discovered a new type of non-CpG methylation in brain cells that is more dynamic and potentially reversible, challenging the idea that methylation changes are permanent. This has implications for better understanding diseases like Rett syndrome that involve methylation enzymes. Both studies provide insights with potential medical applications like new cancer prevention or treatment strategies.
The document discusses transcription and RNA processing. It summarizes two scientific articles about regulating DNA transcription in bacteria and accessing DNA in mitochondria to treat disease. The first article finds that a riboswitch can regulate transcription in bacteria and may be a target for new antibiotics. The second discovers compounds that can access mitochondrial DNA to silence genes associated with nerve and muscle diseases. The medical utility section argues that further research on transcription and RNA processing could provide new treatments for common neurological disorders and address the growing problem of antibiotic resistance.
1) Scientists have reconstituted the DNA "replication fork" for the first time, allowing them to study the complex process of DNA duplication.
2) Researchers discovered that an enzyme involved in metabolizing carbohydrates, pyruvate dehydrogenase complex (PDC), is present in the nucleus and can acetylate histones to regulate DNA replication and gene expression.
3) Understanding how DNA replicates and is regulated could help scientists develop treatments for diseases like cancer by controlling genetic and epigenetic processes involved in uncontrolled cell growth.
Replication Fork and Sweet Genes(Molecular Biology Folding)Ana Cristina Toro
1) Scientists have reconstituted the DNA "replication fork" for the first time, allowing them to study the complex process of DNA duplication.
2) Researchers discovered that an enzyme involved in metabolizing carbohydrates, pyruvate dehydrogenase complex (PDC), is present in the nucleus and can acetylate histones to regulate DNA replication and gene expression.
3) These findings help explain how metabolism and DNA regulation are linked, with potential applications for understanding diseases like cancer where DNA replication is disrupted.
This document summarizes two scientific articles. The first article discusses how the condensin protein folds chromosome arms during cell division in yeast, helping prevent errors. The second article discusses how scientists identified molecular mechanisms behind DNA breakage, a hallmark of cancer cells, finding some DNA regions are more susceptible to damage and cancer results when repair mechanisms fail. The document discusses potential medical applications, like developing new treatments that target these molecules to help prevent genetic disorders and cancers.
The document discusses two discoveries related to repair mechanisms in the body. The first is a discovery using polymer nano-shells that deliver molecules to damaged bone to stimulate the body's own bone cells to repair itself, reducing risks from foreign cells. The second is a Nobel Prize-winning discovery of a DNA repair mechanism failure link to cancer susceptibility, which could help identify high-risk patients and fuel cancer immunotherapy research working with drug companies. Both discoveries are seen as important progress for diseases like cancer and bone injuries that could improve patients' quality of life worldwide.
Three key points from the document:
1. A study by researchers at the University of Oxford found that cells exposed to aldehyde chemicals were unable to adequately repair DNA damage, compared to unexposed cells. This suggests aldehydes cause cancer by reducing DNA repair ability.
2. A separate study by BMJ researchers discovered night shift workers had lower levels of a chemical byproduct of active DNA repair in their urine, indicating their bodies were less able to repair nighttime DNA damage due to suppressed melatonin production.
3. Proper sleep, avoidance of smoking, drinking, and reducing aldehyde exposure through products can help minimize cancer risks by allowing the body to better repair DNA damage on a cellular level
This document summarizes a review article by Dr. Stephen Kron on the relevance and irrelevance of the DNA damage response to radiotherapy. It discusses how scientists have discovered the cellular mechanisms of DNA damage and repair in response to radiation, but there remains a gap in applying this knowledge to improve patient outcomes in radiotherapy. The document also reviews several studies examining factors like tumor hypoxia, oxidative damage, and DNA repair inhibition that influence radiotherapy effectiveness, noting that further research is still needed to better inform clinical practice.
The document discusses two scientific studies. The first study found that a specific stage in the cell cycle (G1 phase) being altered can lead to uncontrolled cell growth and cancer development when telomeres are shortened. The second study discovered that after a heart attack in zebrafish, muscle cells from the undamaged atrium migrated into the damaged ventricle and transformed into ventricular cells, helping regenerate the heart tissue and restore cardiac function.
How to Setup Warehouse & Location in Odoo 17 InventoryCeline George
In this slide, we'll explore how to set up warehouses and locations in Odoo 17 Inventory. This will help us manage our stock effectively, track inventory levels, and streamline warehouse operations.
This document provides an overview of wound healing, its functions, stages, mechanisms, factors affecting it, and complications.
A wound is a break in the integrity of the skin or tissues, which may be associated with disruption of the structure and function.
Healing is the body’s response to injury in an attempt to restore normal structure and functions.
Healing can occur in two ways: Regeneration and Repair
There are 4 phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This document also describes the mechanism of wound healing. Factors that affect healing include infection, uncontrolled diabetes, poor nutrition, age, anemia, the presence of foreign bodies, etc.
Complications of wound healing like infection, hyperpigmentation of scar, contractures, and keloid formation.
This presentation was provided by Racquel Jemison, Ph.D., Christina MacLaughlin, Ph.D., and Paulomi Majumder. Ph.D., all of the American Chemical Society, for the second session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session Two: 'Expanding Pathways to Publishing Careers,' was held June 13, 2024.
Level 3 NCEA - NZ: A Nation In the Making 1872 - 1900 SML.pptHenry Hollis
The History of NZ 1870-1900.
Making of a Nation.
From the NZ Wars to Liberals,
Richard Seddon, George Grey,
Social Laboratory, New Zealand,
Confiscations, Kotahitanga, Kingitanga, Parliament, Suffrage, Repudiation, Economic Change, Agriculture, Gold Mining, Timber, Flax, Sheep, Dairying,
Chapter wise All Notes of First year Basic Civil Engineering.pptxDenish Jangid
Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
The chapter Lifelines of National Economy in Class 10 Geography focuses on the various modes of transportation and communication that play a vital role in the economic development of a country. These lifelines are crucial for the movement of goods, services, and people, thereby connecting different regions and promoting economic activities.
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPRAHUL
This Dissertation explores the particular circumstances of Mirzapur, a region located in the
core of India. Mirzapur, with its varied terrains and abundant biodiversity, offers an optimal
environment for investigating the changes in vegetation cover dynamics. Our study utilizes
advanced technologies such as GIS (Geographic Information Systems) and Remote sensing to
analyze the transformations that have taken place over the course of a decade.
The complex relationship between human activities and the environment has been the focus
of extensive research and worry. As the global community grapples with swift urbanization,
population expansion, and economic progress, the effects on natural ecosystems are becoming
more evident. A crucial element of this impact is the alteration of vegetation cover, which plays a
significant role in maintaining the ecological equilibrium of our planet.Land serves as the foundation for all human activities and provides the necessary materials for
these activities. As the most crucial natural resource, its utilization by humans results in different
'Land uses,' which are determined by both human activities and the physical characteristics of the
land.
The utilization of land is impacted by human needs and environmental factors. In countries
like India, rapid population growth and the emphasis on extensive resource exploitation can lead
to significant land degradation, adversely affecting the region's land cover.
Therefore, human intervention has significantly influenced land use patterns over many
centuries, evolving its structure over time and space. In the present era, these changes have
accelerated due to factors such as agriculture and urbanization. Information regarding land use and
cover is essential for various planning and management tasks related to the Earth's surface,
providing crucial environmental data for scientific, resource management, policy purposes, and
diverse human activities.
Accurate understanding of land use and cover is imperative for the development planning
of any area. Consequently, a wide range of professionals, including earth system scientists, land
and water managers, and urban planners, are interested in obtaining data on land use and cover
changes, conversion trends, and other related patterns. The spatial dimensions of land use and
cover support policymakers and scientists in making well-informed decisions, as alterations in
these patterns indicate shifts in economic and social conditions. Monitoring such changes with the
help of Advanced technologies like Remote Sensing and Geographic Information Systems is
crucial for coordinated efforts across different administrative levels. Advanced technologies like
Remote Sensing and Geographic Information Systems
9
Changes in vegetation cover refer to variations in the distribution, composition, and overall
structure of plant communities across different temporal and spatial scales. These changes can
occur natural.
ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
Certified as an ISO/IEC 27001: Information Security Management Systems (ISMS) Lead Implementer, Data Protection Officer, and Cyber Risks Analyst, Denis brings a heightened focus on data security, privacy, and cyber resilience to every endeavor.
His expertise extends across a diverse spectrum of reporting, database, and web development applications, underpinned by an exceptional grasp of data storage and virtualization technologies. His proficiency in application testing, database administration, and data cleansing ensures seamless execution of complex projects.
What sets Denis apart is his comprehensive understanding of Business and Systems Analysis technologies, honed through involvement in all phases of the Software Development Lifecycle (SDLC). From meticulous requirements gathering to precise analysis, innovative design, rigorous development, thorough testing, and successful implementation, he has consistently delivered exceptional results.
Throughout his career, he has taken on multifaceted roles, from leading technical project management teams to owning solutions that drive operational excellence. His conscientious and proactive approach is unwavering, whether he is working independently or collaboratively within a team. His ability to connect with colleagues on a personal level underscores his commitment to fostering a harmonious and productive workplace environment.
Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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Walmart Business+ and Spark Good for Nonprofits.pdfTechSoup
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You will hear from Liz Willett, the Head of Nonprofits, and hear about what Walmart is doing to help nonprofits, including Walmart Business and Spark Good. Walmart Business+ is a new offer for nonprofits that offers discounts and also streamlines nonprofits order and expense tracking, saving time and money.
The webinar may also give some examples on how nonprofits can best leverage Walmart Business+.
The event will cover the following::
Walmart Business + (https://business.walmart.com/plus) is a new shopping experience for nonprofits, schools, and local business customers that connects an exclusive online shopping experience to stores. Benefits include free delivery and shipping, a 'Spend Analytics” feature, special discounts, deals and tax-exempt shopping.
Special TechSoup offer for a free 180 days membership, and up to $150 in discounts on eligible orders.
Spark Good (walmart.com/sparkgood) is a charitable platform that enables nonprofits to receive donations directly from customers and associates.
Answers about how you can do more with Walmart!"
2. MEDI CAL
UTILI TY
By: Maria Angélica Zapata
Gonzalez
Molecular Biology
Teacher: Lina Martinez
DNA
REPARATION
BI BLIO GRA PHY
• PLOS. (2017, January 26). Quick-and-dirty
DNA repair sets the stage for smoking-
related lung cancer. ScienceDaily. Retrieved
February 7, 2017 from
www.sciencedaily.com/releases/
2017/01/170126142917.htm
• University of Leed. (2017, January 10).
Suppressing a DNA-repairing protein in
brain could be key to treating aggressive
tumors. ScienceDaily. Retrieved February 7,
2017 from www.sciencedaily.com/releases/
2017/01/170110121046.htm
• Martinez Sanchez, Lina Maria. Biología
Molecular. 7 ed. Medellín: UPB.
Fac.Medicina
Lung and brain problems
are now a step
closer to have a
therapy and a
treatment.
Both news give hope
to patient and medical
personal because now there are more studies.
The utility for this is huge advance about
tumor brain is that scientist can look for
similar proteins all around the body that they
can inhibit it and this will give a treatment
for another cancer or another problem, also
using this protein as a base gives scientists.
About lung cancer, an incredible utility is
that knowing what happens to the cell can be
used to recognize those cells earlier so the
cancer can be treated before it affects the
whole lung or the whole body. Also this is a
pathway to create drugs that inhibits the
wrong reparation, in order to repair just what
is good for the cell
Basically, this gives the world a new way to
look at the cell reparation.
3. DNA reparation tries to help the cell when it
is affected, so she can keep her genome and
she can continue doing the right work for our
body. This process start when the cell
recognizes the problem so she can correct the
damage, and this correction the cell can do it
in different ways, for example Base Excision
Repair (BER), Nucleotide Excision Repair
(NER), the pathway depends on the damage,
in this case, if it is a base or a nucleotide.
Sometimes this reparation is what affects the
cells, and despite affecting it, this wrong
DNA will stay with the daughter cells and it
will make a chain of affected cells.
DNA R EPAIR A ND
LUNG CAN CE R
The second most common form of lung cancer
is the squamous cell carcinoma, which involves
two types of lung stem cells: alveolar
progenitor cells and basal cells and
accumulation of DNA.
How they know it?
The authors took the cells from the lungs of
smokers and studied their genes, cell division
and how the cells repair their DNA.
What did they find?
They found that the basal cells were
doing the wrong work so they where
trying to repair DNA but this was
leading to accumulate it and the
bad thing was that the DNA had
so much errors’.
Student’s opinion
Knowing the cells that lead to this kind of
cancer is an incredible and huge advanced
because it gives the scientists a new way to
look at this problem and it will be much
easier to find the cure
DNA REPAIRING
PROTEIN IN
BRAIN
The most common type of brain tumor and the
most aggressive is the glioblastoma.
At the University of Leeds researchers
found that if they inhibited the
protein RAD51, the cell was going to die.
RAD51 is one of the Glioblastoma Stem Cells
which replicates during the treatment
and the result is resistance to it.
What did they do?
Professor Susan Short at the university explained
that radiotherapy affected the DNA of
the cell but the protein was trying
to repair it from the damage, so if they
inhibited the protein, the DNA could not
repair and the treatment would be more effective.
Do they have any problem?
Yes, they do. This experiment has
never been done in a human, but they
have great expectations.
Student’s opinion
Despite being so dangerous, they should
make the experiment on humans because
tumor's expectations are poor so it would give
people at least a chance to survive.
INTR ODUCTION
4.
INTR ODU CTIO N
NER BER
Process that changes a
thymine dimer so the
DNA strand can keep the
normal sequence.
This process is longer but
more specific, it only
changes an specific base.
5.
QUICK -AND- DIRTY DAN REPAIR SET S
THE S TAGE FO R SM OKING -RELATED
LUNG CANCER
2017, January 26
6. The basal cells where the principal problem. These cells from smokers, has a
patron of replication called ‘transcriptional fingerprint’.
QUICK -AND- DIRTY DAN REPAIR SET S T HE STAGE
FOR SM OKING- RE LATED LUNG CANCER
7.
What leads to
carcinoma is a
mutation because of
the accumulation of
repaired DNA that
the cell was doing.
QUICK -AND- DIRTY DAN REPAIR
SETS THE STAGE F OR SMOKING-
REL ATED L UNG CANCER
This way of
reparation is called
‘’non -
homologous end
joining’’.
8. One of the authors, Asselin - Labat, said that their results
indicate that targeting DNA repair processes could be a a
pathway to prevent and treat lung cancer.
QUICK -AND- DIRTY DAN REPAIR SET S T HE
STAGE FOR S MO KING-RELAT ED LU NG
CANCER
9.
I think, this is an incredible pathway
that shows us that when a cell tries
to repair itself, she can make the
damage and I think this is important
because is a new way to look at the
reparation that is not always trying
to help the cell.
Student’s opinion
10.
SUPPRES SING A DNA-REPAIRING
PROTEIN IN B RA IN COULD BE KEY
TO TREATING AGGRESSIVE TUMORS
2017, January 10
11. SUPPRES SING A DNA-REPAIRING PROT EIN IN BRAIN
COUL D B E KEY TO TREATING AGG RESSI VE TUMORS
RAD51 protein is involved in te reparation of DNA double strand breaks
and helps the cell to grow. But RAD51 is related to decrease
patient survival when they have cancer.
12.
SUP PRES SING A DNA-
REPA IRING P ROT EIN IN
BRA IN COULD BE KEY TO
TREAT ING AGGRESSIVE
How did they find the
protein RAD51 in
glioblastoma cells?
They used
inmunofluorescence
microscopy
13. SUPPRES SING A DNA-REPAIRING PROT EIN IN BRAIN
COUL D B E KEY TO TREATING AGG RESSI VE TUMORS
The people between 45 and 75 years are the most
affected. The time that they stay alive with cancer
is almost 12 - 18 months and only 20% of patients
survive more than one year.
14.
It is important to continue the
experiments because they are really
close to find the cure of a really big
tumor.
Also, the fact that radiotherapy is a
part of the problem can help to find a
different treatment where the help
does not induce a bad DNA repair.
Student’s opinion
16. M E D I C A L U T I L I T Y
DNA reparation could be useful to
correct cells like nervous cell after a
disease where part of the mobility is
lost. If scientists induce the cell to
repair, probably it would help it to
return part of the functioning. Also it
could lead to a treatment with RAD51,
if the try radiotherapy and the cell try
to repair and this could stimulate the
process.
17. M E D I C A L U T I L I T Y
A great utility would be that
scientist can look for similar
tumoral proteins in different cells
so the protein could
accelerate the process of
reparation or
accumulate the DNA
reparation, but a good
one that can help the
cell faster.
18. M E D I C A L U T I L I T Y
Finally, nicotine is what makes the
basal cells start to repair
themselves, so it would be an
advance to find where this
reparation is good for the cell so
nicotine could be a drug so tissues
could be repaired in the moment
that is found the problem so it
won't affect in the same way the
body .
19. BIBLIOGRAP HY
• PLOS. (2017, January 26). Quick-and-dirty DNA repair sets
the stage for smoking-related lung cancer. ScienceDaily.
Retrieved February 7, 2017 from www.sciencedaily.com/
releases/2017/01/170126142917.htm
• University of Leed. (2017, January 10). Suppressing a DNA-
repairing protein in brain could be key to treating
aggressive tumors. ScienceDaily. Retrieved February 7, 2017
from www.sciencedaily.com/releases/
2017/01/170110121046.htm
• Martinez Sanchez, Lina Maria. Biología Molecular. 7 ed.
Medellín: UPB. Fac.Medicina
20. ‘’WHAT I STAND FOR IS
WHAT I STAND ON.’’
- Wenddell Berry