Inflammation is the body's response to injury or infection that helps initiate the healing process. It involves changes in blood vessels and the migration of white blood cells to the injured or infected area. The four main signs of inflammation are redness, heat, swelling, and pain. Chemical mediators released during inflammation, such as histamine and prostaglandins, cause these symptoms by increasing blood flow and vascular permeability. Neutrophils play a key role by migrating to the site of injury or infection and phagocytosing pathogens through a multi-step process involving adhesion, chemotaxis, and activation of intracellular killing mechanisms. The inflammatory response ultimately helps eliminate the injurious stimuli and initiate tissue repair.
The document provides information about inflammation including its causes, classification, and mechanisms. It discusses how inflammation is the body's response to harmful stimuli and can be either acute or chronic. Acute inflammation develops rapidly in response to injury and involves innate immune responses, while chronic inflammation can last months to years and involves adaptive immunity. The key events of acute inflammation are increased blood flow, vascular permeability, and migration of immune cells to the site of injury.
Pathogen recognition and tissue damage initiate an inflammatory response. The response involves localized changes like increased blood flow, vascular permeability, and leukocyte migration. Neutrophils are recruited within hours and macrophages within a day. Together they phagocytose pathogens and release inflammatory mediators, causing pain, swelling and fever. The response helps isolate and remove infection while activating adaptive immunity.
The document summarizes the key steps and processes involved in acute inflammation. It describes how immune cells like macrophages recognize pathogens or damage and release inflammatory mediators. These mediators cause vasodilation, increased permeability, and the classic signs of inflammation - redness, heat, swelling and pain. The document then details the leukocyte adhesion cascade by which immune cells migrate to the site of inflammation, and the processes of chemotaxis, phagocytosis, intracellular killing, and extracellular release involved in the immune response.
Inflammation is characterized by cardinal signs such as redness, swelling, heat, and pain. It involves a complex series of events including increased blood flow, vascular permeability, and migration of leukocytes. Mediators like histamine, cytokines, prostaglandins, and leukotrienes are released from cells to induce and propagate the inflammatory response through effects on blood vessels and immune cells. Acute inflammation resolves within days while chronic inflammation persists long-term and can cause tissue damage.
This document describes inflammation, including its causes, mechanisms, and effects. It defines acute and chronic inflammation and outlines the vascular and cellular events of acute inflammation. This includes increased blood flow, vascular permeability, exudation of fluid, and migration of neutrophils. It also discusses the various chemical mediators involved, such as histamine, prostaglandins, leukotrienes, and cytokines. These mediators cause effects like vasodilation, increased permeability, and chemotaxis. The document notes both local and potential systemic manifestations of inflammation, such as fever, acute phase response, and changes in white blood cell count.
This document provides an overview of inflammation, including its definition, history, types (acute and chronic), classical signs, vascular and cellular events, chemical mediators, and outcomes. Inflammation is defined as a protective response to injury or infection that involves increased blood flow, blood vessel permeability, and the migration of white blood cells. The classical signs of inflammation are heat, redness, swelling, pain, and loss of function. Key events in acute inflammation include increased vascular permeability, chemotaxis of white blood cells, phagocytosis of pathogens, and the release of chemical mediators like histamine and cytokines. Chronic inflammation is long-lasting inflammation that involves ongoing tissue damage and repair. Systemic inflammatory response syndrome (SIRS)
This document summarizes inflammation and the inflammatory response. It describes inflammation as the body's protective response to injury or infection that involves redness, swelling, heat, and pain. There are two main types of inflammation - acute and chronic. Acute inflammation is short-lived while chronic inflammation can last for months or years. The document then outlines the events in the inflammatory response, including the release of inflammatory mediators, vascular changes, recruitment of phagocytic cells, vasodilation, exudation and edema formation, and cell emigration. Key pro-inflammatory and anti-inflammatory cytokines involved in regulating inflammation are also discussed.
Chronic inflammation is inflammation of prolonged duration that can last weeks to years. It is characterized by infiltration of mononuclear cells like macrophages, lymphocytes, and plasma cells. Tissue destruction and repair also occur simultaneously through new vessel proliferation and fibrosis. Common causes include persistent infections that are difficult to clear, immune-mediated diseases where the immune system attacks the body's own tissues, prolonged exposure to toxic substances, and autoimmunity. Chronic inflammation involves macrophages, lymphocytes, and mediators that sustain the inflammatory response.
The document provides information about inflammation including its causes, classification, and mechanisms. It discusses how inflammation is the body's response to harmful stimuli and can be either acute or chronic. Acute inflammation develops rapidly in response to injury and involves innate immune responses, while chronic inflammation can last months to years and involves adaptive immunity. The key events of acute inflammation are increased blood flow, vascular permeability, and migration of immune cells to the site of injury.
Pathogen recognition and tissue damage initiate an inflammatory response. The response involves localized changes like increased blood flow, vascular permeability, and leukocyte migration. Neutrophils are recruited within hours and macrophages within a day. Together they phagocytose pathogens and release inflammatory mediators, causing pain, swelling and fever. The response helps isolate and remove infection while activating adaptive immunity.
The document summarizes the key steps and processes involved in acute inflammation. It describes how immune cells like macrophages recognize pathogens or damage and release inflammatory mediators. These mediators cause vasodilation, increased permeability, and the classic signs of inflammation - redness, heat, swelling and pain. The document then details the leukocyte adhesion cascade by which immune cells migrate to the site of inflammation, and the processes of chemotaxis, phagocytosis, intracellular killing, and extracellular release involved in the immune response.
Inflammation is characterized by cardinal signs such as redness, swelling, heat, and pain. It involves a complex series of events including increased blood flow, vascular permeability, and migration of leukocytes. Mediators like histamine, cytokines, prostaglandins, and leukotrienes are released from cells to induce and propagate the inflammatory response through effects on blood vessels and immune cells. Acute inflammation resolves within days while chronic inflammation persists long-term and can cause tissue damage.
This document describes inflammation, including its causes, mechanisms, and effects. It defines acute and chronic inflammation and outlines the vascular and cellular events of acute inflammation. This includes increased blood flow, vascular permeability, exudation of fluid, and migration of neutrophils. It also discusses the various chemical mediators involved, such as histamine, prostaglandins, leukotrienes, and cytokines. These mediators cause effects like vasodilation, increased permeability, and chemotaxis. The document notes both local and potential systemic manifestations of inflammation, such as fever, acute phase response, and changes in white blood cell count.
This document provides an overview of inflammation, including its definition, history, types (acute and chronic), classical signs, vascular and cellular events, chemical mediators, and outcomes. Inflammation is defined as a protective response to injury or infection that involves increased blood flow, blood vessel permeability, and the migration of white blood cells. The classical signs of inflammation are heat, redness, swelling, pain, and loss of function. Key events in acute inflammation include increased vascular permeability, chemotaxis of white blood cells, phagocytosis of pathogens, and the release of chemical mediators like histamine and cytokines. Chronic inflammation is long-lasting inflammation that involves ongoing tissue damage and repair. Systemic inflammatory response syndrome (SIRS)
This document summarizes inflammation and the inflammatory response. It describes inflammation as the body's protective response to injury or infection that involves redness, swelling, heat, and pain. There are two main types of inflammation - acute and chronic. Acute inflammation is short-lived while chronic inflammation can last for months or years. The document then outlines the events in the inflammatory response, including the release of inflammatory mediators, vascular changes, recruitment of phagocytic cells, vasodilation, exudation and edema formation, and cell emigration. Key pro-inflammatory and anti-inflammatory cytokines involved in regulating inflammation are also discussed.
Chronic inflammation is inflammation of prolonged duration that can last weeks to years. It is characterized by infiltration of mononuclear cells like macrophages, lymphocytes, and plasma cells. Tissue destruction and repair also occur simultaneously through new vessel proliferation and fibrosis. Common causes include persistent infections that are difficult to clear, immune-mediated diseases where the immune system attacks the body's own tissues, prolonged exposure to toxic substances, and autoimmunity. Chronic inflammation involves macrophages, lymphocytes, and mediators that sustain the inflammatory response.
This document summarizes inflammation and the cellular responses involved. It describes inflammation as the body's protective response to injury that is interwoven with the repair process. The cardinal signs of acute inflammation are described as heat, redness, swelling, pain, and loss of function. Both acute and chronic inflammation involve vascular changes, leukocyte migration, and chemical mediators like histamine, cytokines, and arachidonic acid metabolites. Phagocytosis, granulomatous inflammation, healing, and extracellular matrix remodeling are also summarized.
Acute inflammation is the early response of tissue to injury that is typically short-lived. It aims to remove injurious agents and is characterized by five signs: pain, heat, redness, swelling, and loss of function. The vascular components involve increased permeability and blood flow causing redness and heat. Cellular components include leukocytes that migrate into tissues and release inflammatory mediators. The outcome depends on the tissue and injurious agent, and may result in resolution, fibrosis, abscess formation, or chronic inflammation if the agent persists long-term.
This document defines inflammation and its signs, types, and mechanisms. It discusses the vascular and cellular events of acute inflammation, including leukocyte margination, rolling, adhesion, chemotaxis, phagocytosis, and the roles of chemical mediators. Chronic inflammation is characterized by mononuclear cell infiltration and tissue destruction, with possible outcomes of resolution, scarring, or progression to chronicity. Chronic inflammation can be non-specific or granulomatous, the latter forming small lesions composed of epithelioid cells, giant cells, and lymphocytes.
The immune system consists of nonspecific innate immunity and specific acquired immunity. Nonspecific immunity acts as the first line of defense through physical barriers like skin and mucous membranes, and chemical factors like stomach acid and lysozyme. When barriers are breached, inflammation occurs, characterized by redness, swelling, heat, pain, and leads to tissue repair. The second line of defense includes phagocytes that ingest pathogens, the complement system that opsonizes pathogens, and interferons that interfere with viral replication.
This document summarizes a seminar presentation on inflammation given by Manu S J to the Department of Pharmacology at PES College of Pharmacy. It defines inflammation, describes the classic signs of acute inflammation and the pathophysiology involving increased blood flow, vascular permeability, and cellular infiltration. It also discusses causes of inflammation including infection and injury, and the roles of chemical mediators like histamine, cytokines, and complement proteins in propagating the inflammatory response. Chronic inflammation is characterized by prolonged duration and tissue proliferation or destruction. Granulomatous inflammation involves macrophage aggregation forming granulomas.
This document summarizes a seminar on the cascade of inflammation. It discusses the signs of inflammation, inflammatory cells and mediators, types of inflammation including acute and chronic, and the mechanisms and cellular events of acute inflammation. Specifically, it outlines the vascular events of acute inflammation including changes in blood flow and vascular permeability, as well as the cellular events of leucocyte exudation and phagocytosis.
1. The document discusses inflammation and the cellular responses involved. It describes the multiple causes of inflammation and outlines the classic five signs of inflammation: heat, redness, swelling, pain, and loss of function.
2. The summary of the inflammatory process involves four key steps: 1) vasodilation and increased blood flow, 2) increased vascular permeability, 3) leukocyte exudation into tissues, and 4) phagocytosis and killing of pathogens by cells such as neutrophils.
3. Chemical mediators released during inflammation, such as histamine, prostaglandins, and cytokines, help regulate the inflammatory response both locally and systemically.
This document discusses inflammation and wound healing. It begins by defining inflammation as the body's protective response to tissue injury. The causes of inflammation include microbial infections, hypersensitivity reactions, physical trauma, chemicals, and tissue necrosis. The signs of acute inflammation are redness, heat, swelling, pain, and loss of function. Mediators of inflammation such as histamine, prostaglandins, and complement proteins are released in response to injury and stimulate the inflammatory response. This includes increased blood flow, vascular permeability, and recruitment of immune cells to the injured site to clear infection and initiate repair. Both acute and chronic inflammation aim to remove harmful stimuli and initiate healing, though chronic inflammation can lead to fibrosis and tissue damage if the stimulus
Inflammation is the body's response to injury or infection. It involves both vascular changes and cellular events at the site of injury or infection. The vascular changes include transient vasoconstriction, followed by vasodilation and increased vascular permeability, leading to exudation of fluid proteins from blood vessels into tissues. This exudate carries antibodies, complement proteins, and cells to help fight infection and begin repair. The cardinal signs of inflammation - redness, heat, swelling, pain, and loss of function - result from these vascular and cellular processes.
Inflammation can be acute or chronic. Acute inflammation is characterized by rapid onset, short duration, and neutrophil infiltration. The classic signs are redness, swelling, heat, pain, and loss of function. Chemotactic factors recruit neutrophils from the bloodstream into tissues through a multi-step process. Neutrophils then phagocytose pathogens and debris. Chemical mediators like histamine, bradykinin, prostaglandins, and cytokines are released to increase vascular permeability and perpetuate the inflammatory response. Chronic inflammation is long-lasting with lymphocyte and macrophage involvement, potentially progressing to tissue damage if unresolved.
This document discusses inflammation. It defines inflammation as the body's local response to injury or infection aimed at eliminating the cause of injury and initiating repair. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. The early response involves vasodilation and increased permeability, causing swelling. The late response involves neutrophils in acute inflammation and macrophages in chronic cases, which work to destroy pathogens and initiate healing. Understanding inflammation is important for diagnosing conditions like appendicitis and treating diseases.
This document provides an overview of inflammation. It defines inflammation, discusses the cardinal signs of inflammation, and describes the types of inflammation including acute and chronic inflammation. For acute inflammation, it covers the pathogenesis involving changes in vascular flow and permeability and leukocyte emigration. It also discusses the chemical mediators involved in acute inflammation including histamine, prostaglandins, leukotrienes, nitric oxide, cytokines, and complement and coagulation proteins. Chronic inflammation is characterized by infiltration of mononuclear cells like macrophages, lymphocytes, and plasma cells over a prolonged duration.
Acute inflammation is the early response of tissue to injury and is characterized by changes in the microcirculation such as increased fluid exudation and leukocyte emigration from blood vessels to the injured area. It is typically short in duration and aims to remove the injurious agent. The major causes include infections, tissue necrosis, foreign bodies, and burns. Acute inflammation exhibits cardinal signs of pain, heat, redness, swelling, and loss of function and involves vascular changes like increased permeability and blood flow as well as cellular components like leukocytes that release inflammatory mediators. The morphological patterns of acute inflammation depend on the type and extent of tissue response. Outcomes range from resolution to fibrosis, abscess formation, or progression to
The document summarizes inflammatory responses and their role in innate immunity. When barriers like the skin are damaged, resident cells release signals that trigger inflammation - characterized by redness, swelling, heat and pain. This response recruits leukocytes and tries to resolve infection or damage through pathogen clearance and healing. However, chronic inflammation from persistent triggers can lead to long-term issues like arthritis or disease.
INFLAMMATORY RESPONSE IN HUMANS AND IT FUNCTIONssri37388
This document discusses inflammation and its different stages. It describes acute inflammation as a short-term process involving redness, swelling, heat and pain that begins to cease upon removal of the stimulus. Chronic inflammation is inflammation that lasts for months or years and is associated with diseases like diabetes and COPD. The document outlines the vascular, cellular and resolution stages of inflammation, explaining the role of immune cells, cytokines, lipids and other mediators in each phase.
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
The document defines inflammation as the body's response to injury or infection that aims to eliminate the injurious agent and damaged tissues. It lists the four cardinal signs of inflammation as redness, swelling, heat, and pain. The types of inflammation are acute, which is short-lived and involves neutrophils, and chronic, which persists long-term and involves lymphocytes and plasma cells. Chemical mediators released from cells and plasma propagate the inflammatory response.
This document provides an overview of inflammation. It defines inflammation and describes the signs and types, including acute and chronic inflammation. For acute inflammation, it details the vascular events of altered microvasculature, including hemodynamic changes and increased vascular permeability. It also describes the cellular events of exudation of leukocytes and phagocytosis. It lists the chemical mediators of inflammation released by cells and originating from plasma. It discusses the regulation of inflammation and factors determining the inflammatory response. It outlines the morphology, systemic effects, and fate of acute inflammation. It defines chronic inflammation and describes its causes, features, types, histological features, and systemic effects.
The document provides an overview of inflammation, including its definition, etiology, cardinal signs, types (acute and chronic), vascular and cellular events in acute inflammation, mediators, regulation, inflammatory cells, factors affecting acute inflammation, and the fate of acute inflammation. It also discusses chronic inflammation, granulomatous inflammation, comparing acute and chronic inflammation, and dental implications including pulpal infections, periapical infections/inflammation, gingival inflammation, and periodontal inflammation.
A Visual Guide to 1 Samuel | A Tale of Two HeartsSteve Thomason
These slides walk through the story of 1 Samuel. Samuel is the last judge of Israel. The people reject God and want a king. Saul is anointed as the first king, but he is not a good king. David, the shepherd boy is anointed and Saul is envious of him. David shows honor while Saul continues to self destruct.
This document summarizes inflammation and the cellular responses involved. It describes inflammation as the body's protective response to injury that is interwoven with the repair process. The cardinal signs of acute inflammation are described as heat, redness, swelling, pain, and loss of function. Both acute and chronic inflammation involve vascular changes, leukocyte migration, and chemical mediators like histamine, cytokines, and arachidonic acid metabolites. Phagocytosis, granulomatous inflammation, healing, and extracellular matrix remodeling are also summarized.
Acute inflammation is the early response of tissue to injury that is typically short-lived. It aims to remove injurious agents and is characterized by five signs: pain, heat, redness, swelling, and loss of function. The vascular components involve increased permeability and blood flow causing redness and heat. Cellular components include leukocytes that migrate into tissues and release inflammatory mediators. The outcome depends on the tissue and injurious agent, and may result in resolution, fibrosis, abscess formation, or chronic inflammation if the agent persists long-term.
This document defines inflammation and its signs, types, and mechanisms. It discusses the vascular and cellular events of acute inflammation, including leukocyte margination, rolling, adhesion, chemotaxis, phagocytosis, and the roles of chemical mediators. Chronic inflammation is characterized by mononuclear cell infiltration and tissue destruction, with possible outcomes of resolution, scarring, or progression to chronicity. Chronic inflammation can be non-specific or granulomatous, the latter forming small lesions composed of epithelioid cells, giant cells, and lymphocytes.
The immune system consists of nonspecific innate immunity and specific acquired immunity. Nonspecific immunity acts as the first line of defense through physical barriers like skin and mucous membranes, and chemical factors like stomach acid and lysozyme. When barriers are breached, inflammation occurs, characterized by redness, swelling, heat, pain, and leads to tissue repair. The second line of defense includes phagocytes that ingest pathogens, the complement system that opsonizes pathogens, and interferons that interfere with viral replication.
This document summarizes a seminar presentation on inflammation given by Manu S J to the Department of Pharmacology at PES College of Pharmacy. It defines inflammation, describes the classic signs of acute inflammation and the pathophysiology involving increased blood flow, vascular permeability, and cellular infiltration. It also discusses causes of inflammation including infection and injury, and the roles of chemical mediators like histamine, cytokines, and complement proteins in propagating the inflammatory response. Chronic inflammation is characterized by prolonged duration and tissue proliferation or destruction. Granulomatous inflammation involves macrophage aggregation forming granulomas.
This document summarizes a seminar on the cascade of inflammation. It discusses the signs of inflammation, inflammatory cells and mediators, types of inflammation including acute and chronic, and the mechanisms and cellular events of acute inflammation. Specifically, it outlines the vascular events of acute inflammation including changes in blood flow and vascular permeability, as well as the cellular events of leucocyte exudation and phagocytosis.
1. The document discusses inflammation and the cellular responses involved. It describes the multiple causes of inflammation and outlines the classic five signs of inflammation: heat, redness, swelling, pain, and loss of function.
2. The summary of the inflammatory process involves four key steps: 1) vasodilation and increased blood flow, 2) increased vascular permeability, 3) leukocyte exudation into tissues, and 4) phagocytosis and killing of pathogens by cells such as neutrophils.
3. Chemical mediators released during inflammation, such as histamine, prostaglandins, and cytokines, help regulate the inflammatory response both locally and systemically.
This document discusses inflammation and wound healing. It begins by defining inflammation as the body's protective response to tissue injury. The causes of inflammation include microbial infections, hypersensitivity reactions, physical trauma, chemicals, and tissue necrosis. The signs of acute inflammation are redness, heat, swelling, pain, and loss of function. Mediators of inflammation such as histamine, prostaglandins, and complement proteins are released in response to injury and stimulate the inflammatory response. This includes increased blood flow, vascular permeability, and recruitment of immune cells to the injured site to clear infection and initiate repair. Both acute and chronic inflammation aim to remove harmful stimuli and initiate healing, though chronic inflammation can lead to fibrosis and tissue damage if the stimulus
Inflammation is the body's response to injury or infection. It involves both vascular changes and cellular events at the site of injury or infection. The vascular changes include transient vasoconstriction, followed by vasodilation and increased vascular permeability, leading to exudation of fluid proteins from blood vessels into tissues. This exudate carries antibodies, complement proteins, and cells to help fight infection and begin repair. The cardinal signs of inflammation - redness, heat, swelling, pain, and loss of function - result from these vascular and cellular processes.
Inflammation can be acute or chronic. Acute inflammation is characterized by rapid onset, short duration, and neutrophil infiltration. The classic signs are redness, swelling, heat, pain, and loss of function. Chemotactic factors recruit neutrophils from the bloodstream into tissues through a multi-step process. Neutrophils then phagocytose pathogens and debris. Chemical mediators like histamine, bradykinin, prostaglandins, and cytokines are released to increase vascular permeability and perpetuate the inflammatory response. Chronic inflammation is long-lasting with lymphocyte and macrophage involvement, potentially progressing to tissue damage if unresolved.
This document discusses inflammation. It defines inflammation as the body's local response to injury or infection aimed at eliminating the cause of injury and initiating repair. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. The early response involves vasodilation and increased permeability, causing swelling. The late response involves neutrophils in acute inflammation and macrophages in chronic cases, which work to destroy pathogens and initiate healing. Understanding inflammation is important for diagnosing conditions like appendicitis and treating diseases.
This document provides an overview of inflammation. It defines inflammation, discusses the cardinal signs of inflammation, and describes the types of inflammation including acute and chronic inflammation. For acute inflammation, it covers the pathogenesis involving changes in vascular flow and permeability and leukocyte emigration. It also discusses the chemical mediators involved in acute inflammation including histamine, prostaglandins, leukotrienes, nitric oxide, cytokines, and complement and coagulation proteins. Chronic inflammation is characterized by infiltration of mononuclear cells like macrophages, lymphocytes, and plasma cells over a prolonged duration.
Acute inflammation is the early response of tissue to injury and is characterized by changes in the microcirculation such as increased fluid exudation and leukocyte emigration from blood vessels to the injured area. It is typically short in duration and aims to remove the injurious agent. The major causes include infections, tissue necrosis, foreign bodies, and burns. Acute inflammation exhibits cardinal signs of pain, heat, redness, swelling, and loss of function and involves vascular changes like increased permeability and blood flow as well as cellular components like leukocytes that release inflammatory mediators. The morphological patterns of acute inflammation depend on the type and extent of tissue response. Outcomes range from resolution to fibrosis, abscess formation, or progression to
The document summarizes inflammatory responses and their role in innate immunity. When barriers like the skin are damaged, resident cells release signals that trigger inflammation - characterized by redness, swelling, heat and pain. This response recruits leukocytes and tries to resolve infection or damage through pathogen clearance and healing. However, chronic inflammation from persistent triggers can lead to long-term issues like arthritis or disease.
INFLAMMATORY RESPONSE IN HUMANS AND IT FUNCTIONssri37388
This document discusses inflammation and its different stages. It describes acute inflammation as a short-term process involving redness, swelling, heat and pain that begins to cease upon removal of the stimulus. Chronic inflammation is inflammation that lasts for months or years and is associated with diseases like diabetes and COPD. The document outlines the vascular, cellular and resolution stages of inflammation, explaining the role of immune cells, cytokines, lipids and other mediators in each phase.
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
The document defines inflammation as the body's response to injury or infection that aims to eliminate the injurious agent and damaged tissues. It lists the four cardinal signs of inflammation as redness, swelling, heat, and pain. The types of inflammation are acute, which is short-lived and involves neutrophils, and chronic, which persists long-term and involves lymphocytes and plasma cells. Chemical mediators released from cells and plasma propagate the inflammatory response.
This document provides an overview of inflammation. It defines inflammation and describes the signs and types, including acute and chronic inflammation. For acute inflammation, it details the vascular events of altered microvasculature, including hemodynamic changes and increased vascular permeability. It also describes the cellular events of exudation of leukocytes and phagocytosis. It lists the chemical mediators of inflammation released by cells and originating from plasma. It discusses the regulation of inflammation and factors determining the inflammatory response. It outlines the morphology, systemic effects, and fate of acute inflammation. It defines chronic inflammation and describes its causes, features, types, histological features, and systemic effects.
The document provides an overview of inflammation, including its definition, etiology, cardinal signs, types (acute and chronic), vascular and cellular events in acute inflammation, mediators, regulation, inflammatory cells, factors affecting acute inflammation, and the fate of acute inflammation. It also discusses chronic inflammation, granulomatous inflammation, comparing acute and chronic inflammation, and dental implications including pulpal infections, periapical infections/inflammation, gingival inflammation, and periodontal inflammation.
A Visual Guide to 1 Samuel | A Tale of Two HeartsSteve Thomason
These slides walk through the story of 1 Samuel. Samuel is the last judge of Israel. The people reject God and want a king. Saul is anointed as the first king, but he is not a good king. David, the shepherd boy is anointed and Saul is envious of him. David shows honor while Saul continues to self destruct.
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.
Beyond Degrees - Empowering the Workforce in the Context of Skills-First.pptxEduSkills OECD
Iván Bornacelly, Policy Analyst at the OECD Centre for Skills, OECD, presents at the webinar 'Tackling job market gaps with a skills-first approach' on 12 June 2024
How to Make a Field Mandatory in Odoo 17Celine George
In Odoo, making a field required can be done through both Python code and XML views. When you set the required attribute to True in Python code, it makes the field required across all views where it's used. Conversely, when you set the required attribute in XML views, it makes the field required only in the context of that particular view.
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
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.
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UP
INFLAMMATION @.docx
1. INFLAMMATION:-
1.What is Inflammation ?
Inflammation is a response triggered by damage to living tissues.
The inflammatory response is a defense mechanism that evolved in
higher organisms to protect them from infection and injury.
Its purpose is to localize and eliminate the injurious agent and to remove
damaged tissue components so that the body can begin to heal.
The response consists of changes in blood flow, an increase in
permeability of blood vessels, and the migration of fluid, proteins, and
white blood cells (leukocytes) from the circulation to the site of tissue
damage.
An inflammatory response that lasts only a few days is called acute
inflammation, while a response of longer duration is referred to as
chronic inflammation.
Causes:-
The factors that can stimulate inflammation include microorganisms,
physical agents, chemicals, inappropriate immunological responses, and
tissue death.
Infectious agents such as viruses and bacteria are some of the most
common stimuli of inflammation. Viruses give rise to inflammation by
entering and destroying cells of the body; bacteria release substances
called endotoxins that can initiate inflammation.
Physical trauma, burns, radiation injury, and frostbite can damage
tissues and also bring about inflammation, as can corrosive chemicals
such as acids, alkalis, and oxidizing agents.
As , malfunctioning immunological responses can incite an
inappropriate and damaging inflammatory response. Inflammation can
also result when tissues die from a lack of oxygen or nutrients, a
situation that often is caused by loss of blood flow to the area.
2. Signs
The four cardinal signs of inflammation—redness
(Latin rubor), heat (calor), swelling (tumor), and pain (dolor)—were
described in the 1st century AD by the Roman medical writer Aulus
Cornelius Celsus.
Redness is caused by the dilation of small blood vessels in the area of
injury.
Heat results from increased blood flow through the area and is
experienced only in peripheral parts of the body such as the skin.
Fever is brought about by chemical mediators of inflammation and
contributes to the rise in temperature at the injury.
Swelling, called edema, is caused primarily by the accumulation of fluid
outside the blood vessels.
The pain associated with inflammation results in part from the distortion
of tissues caused by edema, and it also is induced by certain chemical
mediators of inflammation, such as bradykinin, serotonin, and
the prostaglandins.
A fifth consequence of inflammation is the loss of function of the inflamed
area, a feature noted by German pathologist Rudolf Virchow in the 19th
century. Loss of function may result from pain that inhibits mobility or
from severe swelling that prevents movement in the area.
Chemical mediators of inflammation
Although injury starts the inflammatory response, chemical factors
released upon this stimulation bring about the vascular and cellular
changes outlined above. The chemicals originate primarily from
blood plasma, white blood cells (basophils, neutrophils, monocytes, and
macrophages), platelets, mast cells, endothelial cells lining the blood
vessels, and damaged tissue cells.
One of the best-known chemical mediators released from cells during
inflammation is histamine, which triggers vasodilation and increases
vascular permeability. Stored in granules of circulating basophils and mast
cells, histamine is released immediately when these cells are injured.
3. Other substances involved in increasing vascular permeability are
lysosomal compounds, which are released from neutrophils, and certain
small proteins in the complement system, namely C3a and C5a.
Many cytokines secreted by cells involved in inflammation also have
vasoactive and chemotactic properties.
The prostaglandins are a group of fatty acids produced by many types of
cells. Some prostaglandins increase the effects of other substances that
promote vascular permeability. Others affect the aggregation of platelets,
which is part of the clotting process. Prostaglandins are associated with
the pain and fever of inflammation. Prostaglandins are synthesized from
arachidonic acid, as are the leukotrienes, another group of chemical
mediators that have vasoactive properties.
The plasma contains four interrelated systems of proteins—complement,
the kinins, coagulation factors, and the fibrinolytic system—that generate
various mediators of inflammation.
Activated complement proteins serve as chemotactic factors for
neutrophils, increase vascular permeability, and stimulate the release of
histamine from mast cells. They also adhere to the surface of bacteria,
making them easier targets for phagocytes.
The kinin system, which is activated by coagulation factor XII, produces
substances that increase vascular permeability. The most important of the
kinins is bradykinin, which is responsible for much of the pain and itching
experienced with inflammation.
The coagulation system converts the plasma protein fibrinogen into fibrin,
which is a major component of the fluid exudate. The fibrinolytic system
contributes to inflammation primarily through the formation of plasmin,
which breaks down fibrin into products that affect vascular permeability.
Process:-
In response to any harmful or foreign molecule, inflammation generally starts
within few minutes by activation of immune system . Innate system comprises
immune cells that include lymphocytes, dendritic cells (DC’s), neutrophils,
macrophages and mast cells that play significant functions in inflammatory
reactions.
4. 1. Firstly, the pathogens get adhere to particular receptors i.e. G-protein
attached receptors ,Pattern realization receptors and Chemokine
receptors .
2. The fabrication of the inflammatory cytokines including IL-1, IL-6,
chemokines and TNF is initiated by these receptors. These inducers
quickly change the vascular endothelial permissibility and releases
antibodies, complement factors and neutrophils in the site of septicity.
[The inflammatory cytokines increases the excretion of coagulation factors and
C-reactive protein by means of the liver cell. They invoke brain endothelium
and smooth the secretion of prostaglandins. They are important for the key
symptoms of pain and fever via their detrimental effects on CNS (central
nervous system) . Alternatively the viral contamination follows one kind of
signaling pathway via producing different type of cytokines known as type1
interferons (IFN’s). Furthermore, parasitic infections and allergens invoke the
assembly of other inflammatory cytokines IL-13, IL-5, and histamine where the
rest of the pathway is nearly the same .
Inflammation is a complex biochemical mechanism which leads to the
stimulation of infectious agents and promotes injury. It causes tissue damage
and pain monitored through treatment .Chemical agents are secreted by
immune cells like cytokines, chemokine and reactive oxygen species at injury
site to eliminate pathogens. A major constituent of inflammatory process is
arachidonic acid which is a by product of fast acting cell membrane.
Arachidonic acid is transformed into prostaglandins and thromboxane enzyme
by cyclooxygenase (COX).]
3. Neutrophil:-
1. Leukocyte margination and endothelial adhesion:-
Neutrophils begin to attach strongly to the endothelium by using carbohydrate
ligands to show symptoms of inflammation. Endothelial cells in their
stimulated form are responsible for the production of surface bonded and
soluble particles. They produce a strong adhesion between neutrophils and
endothelium.
5. 2.Migration across the endothelium, known as transmigration, via
the process of diapedesis:
Chemokine gradients stimulate the adhered leukocytes to move
between adjacent endothelial cells. The endothelial cells retract and the
leukocytes pass through the basement membrane into the surrounding
tissue .(Neutrophils leave the bloodstream and travels across endothelium . )
3.Movement of leukocytes within the tissue via chemotaxis:
Leukocytes reaching the tissue interstitium bind to extracellular
matrix proteins via expressed integrins and CD44 to prevent them from
leaving the site. A variety of molecules behave as chemoattractants, for
example, C3a or C5, and cause the leukocytes to move along a
chemotactic gradient towards the source of inflammation.
Production of particular cells like cell adhesion molecules (CAMs), their
activators and chemical stimulus is responsible for the neutrophils emigration .
4.Phagocytosis:-
Extravasated neutrophils in the cellular phase come into contact with
microbes at the inflamed tissue. Phagocytes express cell-surface
endocytic pattern recognition receptors (PRRs) that have affinity and
efficacy against non-specific microbe-associated molecular
patterns (PAMPs).
Most PAMPs that bind to endocytic PRRs and initiate phagocytosis .
Upon endocytic PRR binding, that endocytoses the plasma membrane
containing the PRR-PAMP complex, and the microbe.
pathways have been implicated to traffic the endocytosed phagosome
to intracellular lysosomes, where fusion of the phagosome and the
lysosome produces a phagolysosome. The reactive oxygen
species, superoxides and hypochlorite bleach within the
phagolysosomes then kill microbes inside the phagocyte.
Phagocytic efficacy can be enhanced by opsonization. Plasma derived
complement C3b and antibodies that exude into the inflamed tissue
during the vascular phase bind to and coat the microbial antigens. As
well as endocytic PRRs, phagocytes also express opsonin receptors Fc
receptor and complement receptor 1 (CR1), which bind to antibodies
6. and C3b, respectively. The co-stimulation of endocytic PRR and opsonin
receptor increases the efficacy of the phagocytic process, enhancing
the lysosomal elimination of the infective agent.
Molecular or cellular actions of infectious response tend to increase blood
movement, capillary damage, leukocytes access and the creation of chemical
agents . Stimulation of these chemical agents initiates the formation of
inflammatory cytokines including TNF, IL-1, chemokines and IL-6 that causes
tissue damage.
5.Due to phagocytic activity of cells, migratory neutrophils are eventually
removed from inflammatory site through apoptosis and produce anti-
inflammatory cytokines .