KANDAKUMAR S (KK) Molecular Oncology Lab (MOL) seminar
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The document discusses multistep carcinogenesis and the molecular basis of cancer development. It notes that cancer develops through multiple genetic changes over time, involving alterations in proto-oncogenes and tumor suppressor genes. This allows cancer cells to evade growth controls and develop properties like sustained angiogenesis and metastasis. A key example is the multistep progression of colon cancer through changes in the APC, RAS, and P53 genes.
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Biologia del Cancer
The document discusses several key aspects of cancer biology including:
1) Tumorigenesis is a multi-step process that begins with initial genetic changes in cells and progresses to increased proliferation, decreased cell death, and further genetic alterations.
2) Cancers evolve and progress through primary tumor formation, transformation, metastasis, and tumor evolution at distant sites in the body influenced by anatomical and microenvironment factors.
3) Angiogenesis, the formation of new blood vessels, is required to establish metastases and is mediated by growth factors released by tumor and host cells.
Hall marks of Cancer
Cancer is characterized by abnormal cell growth and division. The hallmarks of cancer include self-sufficiency in growth signals, insensitivity to growth inhibition, evading apoptosis, limitless replicative potential, sustained angiogenesis, and ability to invade and metastasize. Cancer results from mutations in oncogenes and tumor suppressor genes caused by factors such as viruses, bacteria, chemicals, and radiation.
Hallmarks in cancer
The document discusses the hallmarks of cancer. It describes six fundamental changes or hallmarks in cancer cells that allow them to grow uncontrollably and potentially spread throughout the body. These hallmarks are: self-sufficiency in growth signals, insensitivity to anti-growth signals, evading programmed cell death (apoptosis), limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. The document provides details on each of these hallmarks and how they enable cancerous behavior in cells.
Pathophysiology of cancer spread
Cancer progression involves multiple physiological changes that allow tumor cells to proliferate uncontrollably, evade growth suppression, resist cell death, replicate indefinitely, induce angiogenesis, and activate invasion and metastasis. Key mechanisms driving these changes include autocrine and paracrine signaling, alterations in growth factor pathways and overexpression of receptors, evading tumor suppressors like pRb, resisting apoptosis through pathways like Bcl-2, maintaining telomere length for replicative immortality, inducing angiogenesis through VEGF/FGF, and activating invasion through degradation of extracellular matrix and cell adhesion changes.
Cancer biochemistry
Cancer develops through a process called carcinogenesis where normal cells are transformed into cancer cells through genetic and epigenetic mutations. These mutations activate oncogenes and inactivate tumor suppressor genes, altering the biochemistry of the cell and causing uncontrolled cell growth. The mutations disrupt the typical cell division and growth factor signaling pathways, leading cells to proliferate autonomously without dependence on external growth signals. Common alterations include overproduction of growth factors, changes to growth factor receptors and intracellular signaling proteins, and autocrine signaling loops.
Oncoproteins
Tumour markers can play a crucial role in detecting cancer and assessing response to therapy. They are substances produced either by tumour cells or by the body in response to cancer. Oncoproteins are proteins encoded by oncogenes which normally maintain a fine balance between cell proliferation and differentiation but become permanently activated in cancer, stimulating cell growth. Elevated levels of various oncoproteins and other tumour markers can be detected in blood and other body fluids, serving as biomarkers for early cancer detection and prediction of prognosis. Common tumour markers discussed include AFP, CEA, CA19-9, CA15-3, CA125, and proteins associated with growth factors, receptors, and cellular signalling pathways.
cancer
The document describes the nCounter Analysis System, a technology for multiplexed digital detection of target molecules without compromising data quality or quantity. Key points:
- It allows multiplexing of up to 800 targets in a single tube with a simple workflow and automated processing requiring only 15 minutes of hands-on time.
- Data output includes target identifiers, count numbers, and internal controls, enabling high quantitative reproducibility across assays.
- The system directly assays tissue, cell, and blood lysates as well as FFPE samples with no need for amplification, reverse transcription, or sample partitioning.
Pathophysiology of breast cancer (2)
1) Genetic mutations can cause unregulated cell growth and proliferation leading to the formation of malignant breast tumors.
2) The tumors compress blood vessels reducing blood supply, causing tissue ischemia, necrosis and pain.
3) Cancer cells can spread locally through lymphatic vessels to lymph nodes, where they may form palpable, hard masses.
Recommended
Biologia del Cancer
The document discusses several key aspects of cancer biology including:
1) Tumorigenesis is a multi-step process that begins with initial genetic changes in cells and progresses to increased proliferation, decreased cell death, and further genetic alterations.
2) Cancers evolve and progress through primary tumor formation, transformation, metastasis, and tumor evolution at distant sites in the body influenced by anatomical and microenvironment factors.
3) Angiogenesis, the formation of new blood vessels, is required to establish metastases and is mediated by growth factors released by tumor and host cells.
Hall marks of Cancer
Cancer is characterized by abnormal cell growth and division. The hallmarks of cancer include self-sufficiency in growth signals, insensitivity to growth inhibition, evading apoptosis, limitless replicative potential, sustained angiogenesis, and ability to invade and metastasize. Cancer results from mutations in oncogenes and tumor suppressor genes caused by factors such as viruses, bacteria, chemicals, and radiation.
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Pathophysiology of cancer spread
Cancer progression involves multiple physiological changes that allow tumor cells to proliferate uncontrollably, evade growth suppression, resist cell death, replicate indefinitely, induce angiogenesis, and activate invasion and metastasis. Key mechanisms driving these changes include autocrine and paracrine signaling, alterations in growth factor pathways and overexpression of receptors, evading tumor suppressors like pRb, resisting apoptosis through pathways like Bcl-2, maintaining telomere length for replicative immortality, inducing angiogenesis through VEGF/FGF, and activating invasion through degradation of extracellular matrix and cell adhesion changes.
Cancer biochemistry
Cancer develops through a process called carcinogenesis where normal cells are transformed into cancer cells through genetic and epigenetic mutations. These mutations activate oncogenes and inactivate tumor suppressor genes, altering the biochemistry of the cell and causing uncontrolled cell growth. The mutations disrupt the typical cell division and growth factor signaling pathways, leading cells to proliferate autonomously without dependence on external growth signals. Common alterations include overproduction of growth factors, changes to growth factor receptors and intracellular signaling proteins, and autocrine signaling loops.
Oncoproteins
Tumour markers can play a crucial role in detecting cancer and assessing response to therapy. They are substances produced either by tumour cells or by the body in response to cancer. Oncoproteins are proteins encoded by oncogenes which normally maintain a fine balance between cell proliferation and differentiation but become permanently activated in cancer, stimulating cell growth. Elevated levels of various oncoproteins and other tumour markers can be detected in blood and other body fluids, serving as biomarkers for early cancer detection and prediction of prognosis. Common tumour markers discussed include AFP, CEA, CA19-9, CA15-3, CA125, and proteins associated with growth factors, receptors, and cellular signalling pathways.
cancer
The document describes the nCounter Analysis System, a technology for multiplexed digital detection of target molecules without compromising data quality or quantity. Key points:
- It allows multiplexing of up to 800 targets in a single tube with a simple workflow and automated processing requiring only 15 minutes of hands-on time.
- Data output includes target identifiers, count numbers, and internal controls, enabling high quantitative reproducibility across assays.
- The system directly assays tissue, cell, and blood lysates as well as FFPE samples with no need for amplification, reverse transcription, or sample partitioning.
Pathophysiology of breast cancer (2)
1) Genetic mutations can cause unregulated cell growth and proliferation leading to the formation of malignant breast tumors.
2) The tumors compress blood vessels reducing blood supply, causing tissue ischemia, necrosis and pain.
3) Cancer cells can spread locally through lymphatic vessels to lymph nodes, where they may form palpable, hard masses.
Neoplasia 3
The document discusses several key hallmarks of cancer cells including evading apoptosis, achieving limitless replicative potential through telomerase activation, inducing angiogenesis, and developing the ability to invade locally and metastasize. It describes the intrinsic and extrinsic pathways of apoptosis evasion in cancer cells as well as mechanisms of telomere maintenance, angiogenesis induction, extracellular matrix degradation, vascular dissemination, and homing to distant sites.
Basic concept of Cancer and cancer cell.
Cancer is a genetic disease caused by alterations in genes that can result from mutations during cell division, exposure to external agents, or randomly. There are four main types of cancer - carcinomas, sarcomas, lymphomas, and leukemias. Cancer is characterized by cellular changes that promote uncontrolled growth. Some key cancer genes include oncogenes that promote growth and tumor suppressor genes that normally inhibit growth. Examples are discussed like MYC, RAS, P53, and RB. New strategies to treat cancer focus on immunotherapy, inhibiting cancer-promoting proteins, and blocking angiogenesis within tumors.
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The document summarizes a presentation on the biology of cancer. It discusses the characteristics of cancer cells, including uncontrolled proliferation and avoidance of apoptosis. It describes different types of cancer classified by position and tissue of origin. The document outlines some of the known causes of cancer including physical, chemical, and biological agents as well as genetic factors. It discusses important cancer-related genes such as oncogenes like ras that promote cancer when mutated, and tumor suppressor genes like p53 and Rb that normally prevent cancer when functioning properly. The presentation covers topics such as molecular basis of cancer, etiology, normal cells versus cancer cells, and treatments.
biology of cancer
This document provides an overview of cancer biology. It defines cancer as the abnormal proliferation of cells and discusses the study of cancer (oncology). The document outlines the different types of tumors and cancers based on cell type and tissue of origin. It also explores the causes of cancer including radiation, chemicals and viruses. Key properties of cancer cells like lack of contact inhibition and defective differentiation are examined. The roles of oncogenes and tumor suppressor genes in cancer development are described. The document concludes with a review of cancer treatment methods such as surgery, chemotherapy, radiation therapy and prevention strategies.
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Neoplasia refers to abnormal cell growth or tumors. There are two main types of neoplasia - benign and malignant. Benign tumors remain localized and are non-invasive, while malignant tumors can invade surrounding tissues and spread to distant sites through lymphatic vessels or blood vessels in a process called metastasis. The development of cancer is a multistep process that involves genetic mutations that activate oncogenes and inactivate tumor suppressor genes, resulting in uncontrolled cell growth and division. Key hallmarks of cancer include self-sufficiency in growth signals, insensitivity to growth inhibitory signals, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, and ability to invade and metastasize.
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- It defines liver cancer and describes the two main types - primary (hepatocellular carcinoma and bile duct cancer) and secondary from other cancers spreading to the liver.
- Risk factors, symptoms, screening tests, staging, treatment options including surgery, transplantation, embolization and targeted therapy are summarized.
Carcinogenesis
Cancer develops through a multi-step process involving genetic mutations that disrupt the normal cell cycle and allow uncontrolled cell growth. The cell cycle is regulated by various proto-oncogenes and tumor suppressor genes. Mutations in these genes, such as activating mutations in proto-oncogenes or loss of function mutations in tumor suppressor genes, can cause cells to ignore growth controls and proliferate unchecked. This can eventually lead to the development of malignant tumors. Common tumor suppressor genes include RB1, TP53, BRCA1, and BRCA2, which are involved in processes like cell cycle regulation and DNA repair. Mutations in these genes increase cancer risk.
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This document provides an overview of cancer biology. It defines cancer as the abnormal proliferation of cells and discusses the study of cancer (oncology). The document outlines the different types of tumors and cancers based on cell type and tissue of origin. It also explores the causes of cancer including radiation, chemicals and viruses. Key properties of cancer cells like lack of contact inhibition and defective differentiation are examined. The roles of oncogenes and tumor suppressor genes in cancer development are described. The document concludes with a review of cancer treatment methods such as surgery, chemotherapy, radiation therapy and prevention strategies.
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Cancer develops through a multi-step process involving genetic mutations that disrupt the normal cell cycle and allow uncontrolled cell growth. The cell cycle is regulated by various proto-oncogenes and tumor suppressor genes. Mutations in these genes, such as activating mutations in proto-oncogenes or loss of function mutations in tumor suppressor genes, can cause cells to ignore growth controls and proliferate unchecked. This can eventually lead to the development of malignant tumors. Common tumor suppressor genes include RB1, TP53, BRCA1, and BRCA2, which are involved in processes like cell cycle regulation and DNA repair. Mutations in these genes increase cancer risk.
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Dr g vassiliou
The document discusses how cancer genomics is transforming cancer diagnosis. Next-generation sequencing technologies are enabling whole genome and exome sequencing of tumors at lower costs. This allows comprehensive genomic profiling of cancers to detect mutations, rearrangements, and biomarkers that provide diagnostic, prognostic and treatment information. However, challenges remain around technology, costs, data analysis and clinical integration. Pathologists will need to adapt training and integrate genomic data into diagnostic reporting to realize the potential of cancer genomics.
Introducing the Prodotis M1-Macrophage Hypothesis of Cancer Metastasis (PMMH)
ancer tumor would metastasize. To find the best answer, we have reviewed the cases from 1889 to 2017 in humans, animals and plants tumors. Metastasis involves a complex series of steps in which cancer cells leave the original tumor site and migrate to other parts of the body. The macrophage type M1, seems the main cause of metastasis in humans and animal cancers. In plants, we have not found any case of metastasis and the reason is that they lack the macrophages. Nearly all metastasis hypothesis cannot bring out the next target tissue by even 80%, however; the most correct hypothesis is James Ewing’s theory which challenged the seed and soil theory and proposed that metastasis occurs purely by anatomic and mechanical routes. By putting together all the findings and data from the mentioned dates, we have put forth a new hypothesis which
13-chap-24-lecture.ppt
This document provides an overview of cancer, including:
1) Cancer is caused by the accumulation of genetic damage over time that leads to uncontrolled cell growth and proliferation. This "multi-hit" model involves mutations in oncogenes and tumor suppressor genes.
2) Cancer cells exhibit altered growth signaling, immortality, invasion/metastasis, and evasion of apoptosis. Tumor progression involves additional mutations that increase aggressiveness.
3) Diagnosis involves examining tissue morphology and karyotyping to identify abnormal cancer cell characteristics. Advanced tumors develop blood vessels to grow larger than 2mm.
13-chap-24-lecture.ppt
This document provides an overview of cancer biology. It discusses how cancer is caused by the accumulation of genetic mutations over time that disrupt normal cell growth regulation. Key points covered include: the genetic and molecular basis of cancer; common properties of cancer cells like uncontrolled growth; the role of oncogenes and tumor suppressor genes; how mutations in growth factors, receptors, and cell cycle regulators can cause cancer; and the multi-hit model of carcinogenesis. The document also examines specific cancer-causing mutations and molecular mechanisms.
13-chap-24-lecture.ppt
This document provides an overview of cancer biology. It discusses how cancer is caused by the accumulation of genetic damage over time, leading to gain-of-function mutations in oncogenes and loss of function in tumor suppressor genes. This disrupts normal cell growth pathways. Cancer cells exhibit uncontrolled growth, loss of differentiation, ability to invade and metastasize. The "multi-hit" model explains how cancers develop through multiple mutations. Specific cancer-causing mutations in growth factors, receptors, cell cycle proteins and other genes are also summarized.
Anticancer.ppt
This document provides an overview of cancer biology. It discusses how cancer is caused by the accumulation of genetic mutations over time that disrupt normal cell growth regulation. Key points covered include: the genetic and molecular basis of cancer; common properties of cancer cells like uncontrolled growth; the role of oncogenes and tumor suppressor genes; how mutations in growth factors, receptors, and cell cycle regulators can cause cancer; and the multi-hit model of carcinogenesis. The document also examines specific cancer-causing mutations and molecular mechanisms.
13-chap-24-lecture.ppt
This document provides an overview of cancer biology. It discusses how cancer is caused by the accumulation of genetic mutations over time that disrupt normal cell growth regulation. Key points covered include: the genetic and molecular basis of cancer; common properties of cancer cells like uncontrolled growth; the role of oncogenes and tumor suppressor genes; how mutations in growth factors, receptors, and cell cycle regulators can cause cancer; and the multi-hit model of carcinogenesis. The document also examines specific cancer-causing mutations and molecular mechanisms.
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原版制作(carleton毕业证书)卡尔顿大学毕业证硕士文凭原版一模一样
原版纸张【微信：741003700 】【(carleton毕业证书)卡尔顿大学毕业证】【微信：741003700 】学位证，留信认证（真实可查，永久存档）offer、雅思、外壳等材料/诚信可靠,可直接看成品样本，帮您解决无法毕业带来的各种难题！外壳，原版制作，诚信可靠，可直接看成品样本。行业标杆！精益求精，诚心合作，真诚制作！多年品质 ,按需精细制作，24小时接单,全套进口原装设备。十五年致力于帮助留学生解决难题，包您满意。
本公司拥有海外各大学样板无数，能完美还原海外各大学 Bachelor Diploma degree, Master Degree Diploma
1:1完美还原海外各大学毕业材料上的工艺：水印，阴影底纹，钢印LOGO烫金烫银，LOGO烫金烫银复合重叠。文字图案浮雕、激光镭射、紫外荧光、温感、复印防伪等防伪工艺。材料咨询办理、认证咨询办理请加学历顾问Q/微741003700
留信网认证的作用:
1:该专业认证可证明留学生真实身份
2:同时对留学生所学专业登记给予评定
3:国家专业人才认证中心颁发入库证书
4:这个认证书并且可以归档倒地方
5:凡事获得留信网入网的信息将会逐步更新到个人身份内，将在公安局网内查询个人身份证信息后，同步读取人才网入库信息
6:个人职称评审加20分
7:个人信誉贷款加10分
8:在国家人才网主办的国家网络招聘大会中纳入资料，供国家高端企业选择人才
bordetella pertussis.................................ppt
Bordettela is a gram negative cocobacilli spread by air born drop let
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Classification
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Masking and demasking reagents
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Calcium gluconate
Complexometric Titration/ chelatometry titration/chelating titration, introduction, Types-
1.Direct Titration
2.Back Titration
3.Replacement Titration
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Indicators/Metal ion indicators/ Metallochromic indicators/pM indicators,
Visual Technique,PM indicators (metallochromic), Indicators of pH, Redox Indicators
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Complex titration with EDTA.
Deep Software Variability and Frictionless Reproducibility
Deep Software Variability and Frictionless ReproducibilityUniversity of Rennes, INSA Rennes, Inria/IRISA, CNRS
The ability to recreate computational results with minimal effort and actionable metrics provides a solid foundation for scientific research and software development. When people can replicate an analysis at the touch of a button using open-source software, open data, and methods to assess and compare proposals, it significantly eases verification of results, engagement with a diverse range of contributors, and progress. However, we have yet to fully achieve this; there are still many sociotechnical frictions.
Inspired by David Donoho's vision, this talk aims to revisit the three crucial pillars of frictionless reproducibility (data sharing, code sharing, and competitive challenges) with the perspective of deep software variability.
Our observation is that multiple layers — hardware, operating systems, third-party libraries, software versions, input data, compile-time options, and parameters — are subject to variability that exacerbates frictions but is also essential for achieving robust, generalizable results and fostering innovation. I will first review the literature, providing evidence of how the complex variability interactions across these layers affect qualitative and quantitative software properties, thereby complicating the reproduction and replication of scientific studies in various fields.
I will then present some software engineering and AI techniques that can support the strategic exploration of variability spaces. These include the use of abstractions and models (e.g., feature models), sampling strategies (e.g., uniform, random), cost-effective measurements (e.g., incremental build of software configurations), and dimensionality reduction methods (e.g., transfer learning, feature selection, software debloating).
I will finally argue that deep variability is both the problem and solution of frictionless reproducibility, calling the software science community to develop new methods and tools to manage variability and foster reproducibility in software systems.
Exposé invité Journées Nationales du GDR GPL 2024
waterlessdyeingtechnolgyusing carbon dioxide chemicalspdf
The technology uses reclaimed CO₂ as the dyeing medium in a closed loop process. When pressurized, CO₂ becomes supercritical (SC-CO₂). In this state CO₂ has a very high solvent power, allowing the dye to dissolve easily.
Unlocking the mysteries of reproduction: Exploring fecundity and gonadosomati...
The pygmy halfbeak Dermogenys colletei, is known for its viviparous nature, this presents an intriguing case of relatively low fecundity, raising questions about potential compensatory reproductive strategies employed by this species. Our study delves into the examination of fecundity and the Gonadosomatic Index (GSI) in the Pygmy Halfbeak, D. colletei (Meisner, 2001), an intriguing viviparous fish indigenous to Sarawak, Borneo. We hypothesize that the Pygmy halfbeak, D. colletei, may exhibit unique reproductive adaptations to offset its low fecundity, thus enhancing its survival and fitness. To address this, we conducted a comprehensive study utilizing 28 mature female specimens of D. colletei, carefully measuring fecundity and GSI to shed light on the reproductive adaptations of this species. Our findings reveal that D. colletei indeed exhibits low fecundity, with a mean of 16.76 ± 2.01, and a mean GSI of 12.83 ± 1.27, providing crucial insights into the reproductive mechanisms at play in this species. These results underscore the existence of unique reproductive strategies in D. colletei, enabling its adaptation and persistence in Borneo's diverse aquatic ecosystems, and call for further ecological research to elucidate these mechanisms. This study lends to a better understanding of viviparous fish in Borneo and contributes to the broader field of aquatic ecology, enhancing our knowledge of species adaptations to unique ecological challenges.
Travis Hills' Endeavors in Minnesota: Fostering Environmental and Economic Pr...
Travis Hills of Minnesota developed a method to convert waste into high-value dry fertilizer, significantly enriching soil quality. By providing farmers with a valuable resource derived from waste, Travis Hills helps enhance farm profitability while promoting environmental stewardship. Travis Hills' sustainable practices lead to cost savings and increased revenue for farmers by improving resource efficiency and reducing waste.
Cytokines and their role in immune regulation.pptx
This presentation covers the content and information on "Cytokines " and their role in immune regulation .
如何办理(uvic毕业证书)维多利亚大学毕业证本科学位证书原版一模一样
原版纸张【微信：741003700 】【(uvic毕业证书)维多利亚大学毕业证】【微信：741003700 】学位证，留信认证（真实可查，永久存档）offer、雅思、外壳等材料/诚信可靠,可直接看成品样本，帮您解决无法毕业带来的各种难题！外壳，原版制作，诚信可靠，可直接看成品样本。行业标杆！精益求精，诚心合作，真诚制作！多年品质 ,按需精细制作，24小时接单,全套进口原装设备。十五年致力于帮助留学生解决难题，包您满意。
本公司拥有海外各大学样板无数，能完美还原海外各大学 Bachelor Diploma degree, Master Degree Diploma
1:1完美还原海外各大学毕业材料上的工艺：水印，阴影底纹，钢印LOGO烫金烫银，LOGO烫金烫银复合重叠。文字图案浮雕、激光镭射、紫外荧光、温感、复印防伪等防伪工艺。材料咨询办理、认证咨询办理请加学历顾问Q/微741003700
留信网认证的作用:
1:该专业认证可证明留学生真实身份
2:同时对留学生所学专业登记给予评定
3:国家专业人才认证中心颁发入库证书
4:这个认证书并且可以归档倒地方
5:凡事获得留信网入网的信息将会逐步更新到个人身份内，将在公安局网内查询个人身份证信息后，同步读取人才网入库信息
6:个人职称评审加20分
7:个人信誉贷款加10分
8:在国家人才网主办的国家网络招聘大会中纳入资料，供国家高端企业选择人才
Immersive Learning That Works: Research Grounding and Paths Forward
We will metaverse into the essence of immersive learning, into its three dimensions and conceptual models. This approach encompasses elements from teaching methodologies to social involvement, through organizational concerns and technologies. Challenging the perception of learning as knowledge transfer, we introduce a 'Uses, Practices & Strategies' model operationalized by the 'Immersive Learning Brain' and ‘Immersion Cube’ frameworks. This approach offers a comprehensive guide through the intricacies of immersive educational experiences and spotlighting research frontiers, along the immersion dimensions of system, narrative, and agency. Our discourse extends to stakeholders beyond the academic sphere, addressing the interests of technologists, instructional designers, and policymakers. We span various contexts, from formal education to organizational transformation to the new horizon of an AI-pervasive society. This keynote aims to unite the iLRN community in a collaborative journey towards a future where immersive learning research and practice coalesce, paving the way for innovative educational research and practice landscapes.
Authoring a personal GPT for your research and practice: How we created the Q...
Thematic analysis in qualitative research is a time-consuming and systematic task, typically done using teams. Team members must ground their activities on common understandings of the major concepts underlying the thematic analysis, and define criteria for its development. However, conceptual misunderstandings, equivocations, and lack of adherence to criteria are challenges to the quality and speed of this process. Given the distributed and uncertain nature of this process, we wondered if the tasks in thematic analysis could be supported by readily available artificial intelligence chatbots. Our early efforts point to potential benefits: not just saving time in the coding process but better adherence to criteria and grounding, by increasing triangulation between humans and artificial intelligence. This tutorial will provide a description and demonstration of the process we followed, as two academic researchers, to develop a custom ChatGPT to assist with qualitative coding in the thematic data analysis process of immersive learning accounts in a survey of the academic literature: QUAL-E Immersive Learning Thematic Analysis Helper. In the hands-on time, participants will try out QUAL-E and develop their ideas for their own qualitative coding ChatGPT. Participants that have the paid ChatGPT Plus subscription can create a draft of their assistants. The organizers will provide course materials and slide deck that participants will be able to utilize to continue development of their custom GPT. The paid subscription to ChatGPT Plus is not required to participate in this workshop, just for trying out personal GPTs during it.
ESR spectroscopy in liquid food and beverages.pptx
With increasing population, people need to rely on packaged food stuffs. Packaging of food materials requires the preservation of food. There are various methods for the treatment of food to preserve them and irradiation treatment of food is one of them. It is the most common and the most harmless method for the food preservation as it does not alter the necessary micronutrients of food materials. Although irradiated food doesn’t cause any harm to the human health but still the quality assessment of food is required to provide consumers with necessary information about the food. ESR spectroscopy is the most sophisticated way to investigate the quality of the food and the free radicals induced during the processing of the food. ESR spin trapping technique is useful for the detection of highly unstable radicals in the food. The antioxidant capability of liquid food and beverages in mainly performed by spin trapping technique.
3D Hybrid PIC simulation of the plasma expansion (ISSS-14)
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Sharlene Leurig - Enabling Onsite Water Use with Net Zero Water
Sharlene Leurig - Enabling Onsite Water Use with Net Zero WaterTexas Alliance of Groundwater Districts
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Phenomics assisted breeding in crop improvement
As the population is increasing and will reach about 9 billion upto 2050. Also due to climate change, it is difficult to meet the food requirement of such a large population. Facing the challenges presented by resource shortages, climate
change, and increasing global population, crop yield and quality need to be improved in a sustainable way over the coming decades. Genetic improvement by breeding is the best way to increase crop productivity. With the rapid progression of functional
genomics, an increasing number of crop genomes have been sequenced and dozens of genes influencing key agronomic traits have been identified. However, current genome sequence information has not been adequately exploited for understanding
the complex characteristics of multiple gene, owing to a lack of crop phenotypic data. Efficient, automatic, and accurate technologies and platforms that can capture phenotypic data that can
be linked to genomics information for crop improvement at all growth stages have become as important as genotyping. Thus,
high-throughput phenotyping has become the major bottleneck restricting crop breeding. Plant phenomics has been defined as the high-throughput, accurate acquisition and analysis of multi-dimensional phenotypes
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and analysis methods, numerous infrastructure platforms have been developed for phenotyping.
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bordetella pertussis.................................ppt
bordetella pertussis.................................ppt
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Deep Software Variability and Frictionless Reproducibility
Deep Software Variability and Frictionless Reproducibility
mô tả các thí nghiệm về đánh giá tác động dòng khí hóa sau đốt
mô tả các thí nghiệm về đánh giá tác động dòng khí hóa sau đốt
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Unlocking the mysteries of reproduction: Exploring fecundity and gonadosomati...
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Travis Hills' Endeavors in Minnesota: Fostering Environmental and Economic Pr...
Cytokines and their role in immune regulation.pptx
Cytokines and their role in immune regulation.pptx
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Immersive Learning That Works: Research Grounding and Paths Forward
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Authoring a personal GPT for your research and practice: How we created the Q...
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ESR spectroscopy in liquid food and beverages.pptx
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Sharlene Leurig - Enabling Onsite Water Use with Net Zero Water
Sharlene Leurig - Enabling Onsite Water Use with Net Zero Water
KANDAKUMAR S (KK) Molecular Oncology Lab (MOL) seminar
- 1. MULTISTEP CARCINOGENESIS Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) KANDAKUMAR S Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Ph.D RESEARCH SCHOLAR PERIYAR UNIVERSITY Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) 16.09.2014
- 2. Molecular Oncology Lab (MOL) Hallmarks of Cancer Six fundamental changes 1. Self sufficiency in growth factors 2. Insensitivity to growth-inhibitory signals 3. Evasion of apoptosis 4. Limitless replicative potential 5. Sustained angiogenesis 6. Ability to invade and metastasize Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) 16.09.2014
- 3. Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) 16.09.2014
- 4. Molecular Oncology Lab (MOL) Molecular Basis of multistep carcinogenesis Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) 16.09.2014
- 5. CARCINOGENESIS Carcinogenesis is a multistep process at both the phenotypic and the genetic levels. CARCINOGENS It starts with a (genetic damage): Environmental Chemical Radiation Viral Inhereted Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) 16.09.2014
- 6. Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) 16.09.2014
- 7. 16.09.2014
- 8. Multistep Carcinogenesis Colon Cancer: APC – RAS – P53 Hyperplasia – Adenoma – Carcinoma Tumor progression and heterogeneity Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) 16.09.2014
- 9. Molecular Basis of multistep carcinogenesis Neoplastic transformation is a progressive process involving multiple “hits” or genetic changes. Accumulation of multiple mutations since we need six fundamental changes Evidence is both Epidemiologic: cancer increase with age Molecular : cancers analyzed show multiple genetic mutations 16.09.2014
- 10. Molecular Basis of multistep carcinogenesis Alterations in DNA cause changes in one or both of the following types of genes: Proto-oncogenes Tumor suppressor genes Best example is colonic cancer APCRAS18qp53 16.09.2014
- 11. Molecular Basis of Multistep Carcinogenesis 16.09.2014
- 12. Molecular Basis of multistep Carcinogenesis 16.09.2014
- 13. Development of Sustained Angiogenesis Tumors cannot enlarge beyond 1-2 mm thickness unless they are vascularized, hypoxia will induce apoptosis by activation of TP53 . Angiogenesis is required for tumor growth & metastasis. Tumor-associated angiogenic factors may be produced by the tumor or by inflammatory cells TP53 inhibit angiogenesis by stimulation of anti-angiogenesis molecules VEGF is under the control of RAS oncogene . Proteases are involved in regulating angiogenic & antiangiogenic factors . 16.09.2014
- 14. Ability to Invade & Metastasize 1)Invasion of extracellular matrix 2)Vascular dissemination & homing of tumor cells 16.09.2014
- 15. Vascular dissemination & homing of tumor cells Tumor cells binds to leukocytes, this protect them from host defense mechanisms Tumor cells adhere to vascular endothelium & pass through BM Site of extravasations & Meyts depends on: -Blood & Lymphatic supply -Organ tropism/adhesion molecules 16.09.2014
- 16. 16.09.2014
- 17. 16.09.2014
- 18. 16.09.2014
- 19. Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) THANK YOU Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) Molecular Oncology Lab (MOL) 16.09.2014
Editor's Notes
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