This is a presentation on the topic of Inflammation and repair, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
Amyloid beta hypothesis and current scenario of clinicalMuhammad Jamal
1) The amyloid β hypothesis proposes that amyloid β clumps in the brain trigger neurodegenerative processes leading to Alzheimer's symptoms. Several drugs have targeted amyloid β but have failed in clinical trials.
2) Phase 3 trials of drugs targeting beta and gamma secretase, which produce amyloid β, showed the drugs either had no effect or worsened cognitive ability compared to placebos.
3) Recent anti-amyloid antibody drugs from Biogen, Eli Lilly, and others have also failed in Phase 3 trials, bringing into question the amyloid β hypothesis as the sole cause of Alzheimer's disease.
The document discusses the role of autophagy in the immune system. It describes how autophagy functions in innate immunity through interactions with pattern recognition receptors like TLRs, NLRs, and RLRs. Autophagy helps clear pathogens and regulate cytokine production. The document also examines the role of autophagy in adaptive immunity, particularly antigen presentation through MHC class I and II pathways. Finally, it explores how autophagy impacts T cell and B cell development and homeostasis.
This document discusses different types of hypersensitivity and immunopathology. It covers four main types of hypersensitivity reactions (Type I-IV) that vary in severity from mild to life-threatening. Type I is an immediate reaction mediated by IgE antibodies and mast cells. Type II involves IgG and IgM antibodies against cell surface antigens. Type III reactions are caused by immune complexes circulating in the bloodstream. Type IV is a delayed hypersensitivity mediated by T cells. The document also discusses autoimmune disease, where the immune system attacks the body's own tissues, and immunodeficiencies that increase susceptibility to infection.
Cell injury can be reversible or irreversible, leading to cell death. Reversible injury involves cellular swelling and fatty change. Irreversible injury results in necrosis or apoptosis. Many factors can cause cell injury, including hypoxia from ischemia, anemia, carbon monoxide poisoning or pulmonary disease. Chemical agents, infectious agents, immunological reactions, genetic defects, nutritional imbalances, physical trauma, radiation, aging, and apoptosis can also lead to cell injury or death.
This is a presentation on the topic of Inflammation and repair, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
Amyloid beta hypothesis and current scenario of clinicalMuhammad Jamal
1) The amyloid β hypothesis proposes that amyloid β clumps in the brain trigger neurodegenerative processes leading to Alzheimer's symptoms. Several drugs have targeted amyloid β but have failed in clinical trials.
2) Phase 3 trials of drugs targeting beta and gamma secretase, which produce amyloid β, showed the drugs either had no effect or worsened cognitive ability compared to placebos.
3) Recent anti-amyloid antibody drugs from Biogen, Eli Lilly, and others have also failed in Phase 3 trials, bringing into question the amyloid β hypothesis as the sole cause of Alzheimer's disease.
The document discusses the role of autophagy in the immune system. It describes how autophagy functions in innate immunity through interactions with pattern recognition receptors like TLRs, NLRs, and RLRs. Autophagy helps clear pathogens and regulate cytokine production. The document also examines the role of autophagy in adaptive immunity, particularly antigen presentation through MHC class I and II pathways. Finally, it explores how autophagy impacts T cell and B cell development and homeostasis.
This document discusses different types of hypersensitivity and immunopathology. It covers four main types of hypersensitivity reactions (Type I-IV) that vary in severity from mild to life-threatening. Type I is an immediate reaction mediated by IgE antibodies and mast cells. Type II involves IgG and IgM antibodies against cell surface antigens. Type III reactions are caused by immune complexes circulating in the bloodstream. Type IV is a delayed hypersensitivity mediated by T cells. The document also discusses autoimmune disease, where the immune system attacks the body's own tissues, and immunodeficiencies that increase susceptibility to infection.
Cell injury can be reversible or irreversible, leading to cell death. Reversible injury involves cellular swelling and fatty change. Irreversible injury results in necrosis or apoptosis. Many factors can cause cell injury, including hypoxia from ischemia, anemia, carbon monoxide poisoning or pulmonary disease. Chemical agents, infectious agents, immunological reactions, genetic defects, nutritional imbalances, physical trauma, radiation, aging, and apoptosis can also lead to cell injury or death.
This document discusses inflammation and repair through regeneration and healing by connective tissue replacement. It begins by categorizing cell types by their regenerative ability and identifying conditions that favor regeneration versus repair. Repair occurs when the extracellular matrix is damaged and involves scar formation. The key stages of repair are inflammation, proliferation of fibroblasts and blood vessels to form granulation tissue, angiogenesis, collagen deposition and tissue remodeling. Factors that influence or impair healing are also reviewed.
This document provides an overview of cell injury and cell death processes presented by Dr. Marc Imhotep Cray. It discusses reversible cell injury mechanisms including hydropic swelling, intracellular accumulations, and cellular adaptation processes. It also covers irreversible cell injury mechanisms of necrosis and apoptosis. Necrosis types such as coagulative, liquefactive, caseous, and fat necrosis are described. The document provides histological images and discusses the cellular and molecular mechanisms involved in different types of cell injury and death.
1) The document discusses complications that can occur during the healing of cutaneous wounds, including deficient scar formation, incisional hernias, hypertrophic scarring, keloid formation, excessive contraction and granulation.
2) It also examines healing in specialized tissues like bone, gastrointestinal tract, nervous system, liver, kidney and muscle. Bone healing involves procallus formation, osseous callus formation and remodeling. Fracture healing complications include fibrous union, non-union and delayed union.
3) Gastrointestinal tract healing depends on the depth of injury, from mucosal erosions and ulcerations to replacement by scar tissue in deeper injuries. Nervous system healing involves gliosis
Chronic inflammation can last for months or years and is driven by macrophages and lymphocytes. It can be caused by persistent infections, autoimmune reactions, and foreign bodies. Activated macrophages and T cells secrete cytokines and growth factors that lead to tissue damage and fibrosis over time. Macrophages and T cells also interact and stimulate each other, prolonging the inflammatory response. Granulomas are clusters of macrophages that form in response to chronic inflammation and surround foreign materials to isolate them.
The document discusses cytokines, which are low-molecular-weight regulatory proteins or glycoproteins secreted by immune cells and other cells. Cytokines play major roles in immune, inflammatory, and hematopoietic systems by binding to specific cell receptors and altering gene expression. They have pleiotropic, redundant, synergistic, antagonistic, and cascading properties. Cytokines are classified into families based on structure and receptors. They signal through receptor families like immunoglobulin, class I and II cytokine receptors, TNF receptor, and chemokine receptors to regulate the immune response.
This document provides an overview of cellular injury and cell death. It discusses the concepts of pathology, adaptation through hypertrophy, atrophy, hyperplasia and metaplasia. Cell injury occurs when stress exceeds a cell's adaptive capacity and can result from hypoxia, toxins, infections or genetic factors. Mitochondrial dysfunction reduces ATP and causes cell swelling. Reversible injuries include cloudy swelling and fatty change. Irreversible injuries include necrosis, which involves membrane rupture and organelle damage, and apoptosis, which is programmed single-cell death. Necrosis causes inflammation while apoptosis does not. The document also covers pathologic calcification and its dystrophic and metastatic forms.
Mesenchymal stem cells (MSCs) show potential in treating various orthopaedic conditions. MSCs can differentiate into bone, cartilage, and other tissues, helping repair fractures and cartilage/meniscus injuries. They also secrete factors that promote angiogenesis, regulate inflammation, and induce tissue regeneration through paracrine effects. Clinical studies show MSCs may effectively treat non-union fractures, osteoarthritis, and femoral head necrosis by differentiating into local tissues or secreting factors that aid repair. However, larger high-quality studies are still needed to confirm efficacy, especially for late-stage conditions.
Xeroderma Pigmentosum (XP) is a rare genetic disorder caused by a defect in nucleotide excision repair that results in an inability to repair UV-induced DNA damage. This leads to skin cancers developing at a very young age after only minimal sun exposure. Signs include severe sunburn, freckling, and development of skin cancers. Diagnosis is based on clinical findings and measuring DNA repair factors. Treatment focuses on protecting the skin from UV exposure and promptly removing cancerous growths. Most patients die young from skin cancers, but increased awareness and protection can improve prognosis.
This document outlines the systemic effects of inflammation, including fever, elevated acute phase proteins, anemia, leukocytosis/leukopenia, sepsis, ARDS, and wasting syndrome. It provides details on the mechanisms and clinical presentations of each effect. For example, it explains that fever occurs due to the effects of pyrogens like prostaglandins on the hypothalamus, while elevated acute phase proteins like C-reactive protein and serum amyloid A are produced in the liver in response to cytokines. Sepsis can lead to disseminated intravascular coagulation, hypoglycemia, and cardiac failure.
Healing occurs through regeneration or repair and involves granulation tissue formation. Regeneration fully replaces damaged tissue, while repair uses scar tissue. Granulation tissue forms within 1-3 days from new blood vessels and fibroblasts, filling wounds within a week. Primary wound healing occurs with minimal tissue loss and a thin scar. Secondary healing involves more tissue loss and granulation, with a substantial scar and possible wound contraction. Factors like infection, foreign bodies, wound size/location, and nutrition influence healing. Complications include deficient or excessive scarring that cause issues like dehiscence, hernias, hypertrophic scarring, and contractures.
Cellular Adaptation
as cells encounter stresses they undergo functional or structural adaptations to maintain viability / homeostasis.
Injury - altered homeostasis
if limits of the adaptive response are exceeded or if adaptation not possible, a sequence of events called cell injury occurs.
Reversible Cell Injury
removal of stress results in complete restoration of structural & functional integrity.
b) Irreversible Cell Injury / Cell Death
if stimulus persists or is severe enough from the start, the cell suffers irreversible cell injury and death.
2 main morphologic patterns: necrosis & apoptosis.
Adaptations are reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment.
Physiologic adaptations are responses of cells to normal stimulation by hormones or endogenous chemical mediators
Pathologic adaptations are responses to stress that allow cells to modulate their structure and function and thus escape injury.
Hypertrophy refers to an increase in the size of cells, that results in an increase in the size of the affected organ
The hypertrophied organ has no new cells, just larger cells.
Types:
a) physiologic b) pathologic
Causes:
a) increased functional demand b) hormonal stimulation
concise lecture with tables and pictures about chronic inflammation, its mediators, mechanism and sequele. Granulomatous inflammation with different types of granulomas along with histopathology pictures and description.
Apoptosis is a controlled, programmed cell death process that is essential for normal development and homeostasis. During apoptosis, cells actively trigger intracellular events that lead to cell fragmentation and phagocytosis without causing inflammation. Apoptosis is distinct from necrosis, which is unregulated cell death caused by external cellular injuries. Key aspects of apoptosis include activation of caspases, DNA fragmentation, and changes to cell membranes that mark cells for phagocytosis. Apoptosis pathways can be triggered by extracellular signals or internal cell damage and are important in development, tissue homeostasis, and diseases like cancer when the process goes awry.
This document discusses potential stem cell sources and treatments for spinal cord injury. It summarizes preclinical studies showing umbilical cord blood cells improve recovery when transplanted shortly after spinal cord injury in rat models. Recent clinical trials have transplanted umbilical cord blood cells into humans with chronic spinal cord injury. The document also discusses that lithium treatment may reinforce regeneration by increasing neurotrophin production and survival of transplanted cells in injured spinal cords. ChinaSCINet is conducting several clinical trials testing lithium and umbilical cord blood cell transplants to treat spinal cord injury.
The document provides an overview of the immune system and inflammation. It discusses the inflammatory response process, including the vascular and cellular stages. It describes the signs of inflammation (rubor, tumor, calor, dolor, functio laesa) and cells involved in inflammation like neutrophils, eosinophils, basophils, and monocytes. It also discusses mediators of inflammation like kinins, complement system, histamine, serotonin, arachidonic acid metabolites, platelet activating factor, cytokines, and nitric oxide. Finally, it covers acute phase response, types of inflammation (acute vs chronic), and factors that influence wound healing.
The document defines and discusses various types of necrosis, or cell death, that can occur in living tissue. It begins by defining necrosis as the localized death of cells or tissue occurring in the living body without chemical message. The document then discusses different mechanisms that can lead to necrosis, including swelling, calcium overload, and free radical damage. It describes various histological changes seen in necrotic cells and tissue at both the light and electron microscopic level. Several types of necrosis are also outlined, such as coagulative, caseous, liquefactive, and gangrenous necrosis. Complications from necrosis and treatments are briefly mentioned at the end.
Acquired immunity involves lymphocytes and develops a slower response to specific microbes. It includes two types: the humoral response which produces antibodies, and the cell-mediated response involving cytotoxic lymphocytes. Memory lymphocytes provide a rapid response upon future exposures to the same antigen. T cells are activated by antigens presented on MHC proteins and perform cytotoxic functions or help coordinate immune responses by activating other cells. B cells are activated by contact with antigens and differentiate into memory B cells or antibody-secreting plasma cells. Antibodies neutralize pathogens or mark them for destruction.
This document summarizes a morning conference case involving a 14-year-old girl with chronic rhinosinusitis and recurrent ear infections. She presented with low immunoglobulin levels, recurrent sinopulmonary infections, and a low number of circulating B cells, consistent with a diagnosis of primary immunodeficiency. Specifically, her condition matches the characteristics of autosomal recessive agammaglobulinemia, which involves a profound loss of all immunoglobulin isotypes. The conference discusses the genetic causes, clinical manifestations, and treatment approach for this form of primary immunodeficiency.
This document discusses inflammation and repair through regeneration and healing by connective tissue replacement. It begins by categorizing cell types by their regenerative ability and identifying conditions that favor regeneration versus repair. Repair occurs when the extracellular matrix is damaged and involves scar formation. The key stages of repair are inflammation, proliferation of fibroblasts and blood vessels to form granulation tissue, angiogenesis, collagen deposition and tissue remodeling. Factors that influence or impair healing are also reviewed.
This document provides an overview of cell injury and cell death processes presented by Dr. Marc Imhotep Cray. It discusses reversible cell injury mechanisms including hydropic swelling, intracellular accumulations, and cellular adaptation processes. It also covers irreversible cell injury mechanisms of necrosis and apoptosis. Necrosis types such as coagulative, liquefactive, caseous, and fat necrosis are described. The document provides histological images and discusses the cellular and molecular mechanisms involved in different types of cell injury and death.
1) The document discusses complications that can occur during the healing of cutaneous wounds, including deficient scar formation, incisional hernias, hypertrophic scarring, keloid formation, excessive contraction and granulation.
2) It also examines healing in specialized tissues like bone, gastrointestinal tract, nervous system, liver, kidney and muscle. Bone healing involves procallus formation, osseous callus formation and remodeling. Fracture healing complications include fibrous union, non-union and delayed union.
3) Gastrointestinal tract healing depends on the depth of injury, from mucosal erosions and ulcerations to replacement by scar tissue in deeper injuries. Nervous system healing involves gliosis
Chronic inflammation can last for months or years and is driven by macrophages and lymphocytes. It can be caused by persistent infections, autoimmune reactions, and foreign bodies. Activated macrophages and T cells secrete cytokines and growth factors that lead to tissue damage and fibrosis over time. Macrophages and T cells also interact and stimulate each other, prolonging the inflammatory response. Granulomas are clusters of macrophages that form in response to chronic inflammation and surround foreign materials to isolate them.
The document discusses cytokines, which are low-molecular-weight regulatory proteins or glycoproteins secreted by immune cells and other cells. Cytokines play major roles in immune, inflammatory, and hematopoietic systems by binding to specific cell receptors and altering gene expression. They have pleiotropic, redundant, synergistic, antagonistic, and cascading properties. Cytokines are classified into families based on structure and receptors. They signal through receptor families like immunoglobulin, class I and II cytokine receptors, TNF receptor, and chemokine receptors to regulate the immune response.
This document provides an overview of cellular injury and cell death. It discusses the concepts of pathology, adaptation through hypertrophy, atrophy, hyperplasia and metaplasia. Cell injury occurs when stress exceeds a cell's adaptive capacity and can result from hypoxia, toxins, infections or genetic factors. Mitochondrial dysfunction reduces ATP and causes cell swelling. Reversible injuries include cloudy swelling and fatty change. Irreversible injuries include necrosis, which involves membrane rupture and organelle damage, and apoptosis, which is programmed single-cell death. Necrosis causes inflammation while apoptosis does not. The document also covers pathologic calcification and its dystrophic and metastatic forms.
Mesenchymal stem cells (MSCs) show potential in treating various orthopaedic conditions. MSCs can differentiate into bone, cartilage, and other tissues, helping repair fractures and cartilage/meniscus injuries. They also secrete factors that promote angiogenesis, regulate inflammation, and induce tissue regeneration through paracrine effects. Clinical studies show MSCs may effectively treat non-union fractures, osteoarthritis, and femoral head necrosis by differentiating into local tissues or secreting factors that aid repair. However, larger high-quality studies are still needed to confirm efficacy, especially for late-stage conditions.
Xeroderma Pigmentosum (XP) is a rare genetic disorder caused by a defect in nucleotide excision repair that results in an inability to repair UV-induced DNA damage. This leads to skin cancers developing at a very young age after only minimal sun exposure. Signs include severe sunburn, freckling, and development of skin cancers. Diagnosis is based on clinical findings and measuring DNA repair factors. Treatment focuses on protecting the skin from UV exposure and promptly removing cancerous growths. Most patients die young from skin cancers, but increased awareness and protection can improve prognosis.
This document outlines the systemic effects of inflammation, including fever, elevated acute phase proteins, anemia, leukocytosis/leukopenia, sepsis, ARDS, and wasting syndrome. It provides details on the mechanisms and clinical presentations of each effect. For example, it explains that fever occurs due to the effects of pyrogens like prostaglandins on the hypothalamus, while elevated acute phase proteins like C-reactive protein and serum amyloid A are produced in the liver in response to cytokines. Sepsis can lead to disseminated intravascular coagulation, hypoglycemia, and cardiac failure.
Healing occurs through regeneration or repair and involves granulation tissue formation. Regeneration fully replaces damaged tissue, while repair uses scar tissue. Granulation tissue forms within 1-3 days from new blood vessels and fibroblasts, filling wounds within a week. Primary wound healing occurs with minimal tissue loss and a thin scar. Secondary healing involves more tissue loss and granulation, with a substantial scar and possible wound contraction. Factors like infection, foreign bodies, wound size/location, and nutrition influence healing. Complications include deficient or excessive scarring that cause issues like dehiscence, hernias, hypertrophic scarring, and contractures.
Cellular Adaptation
as cells encounter stresses they undergo functional or structural adaptations to maintain viability / homeostasis.
Injury - altered homeostasis
if limits of the adaptive response are exceeded or if adaptation not possible, a sequence of events called cell injury occurs.
Reversible Cell Injury
removal of stress results in complete restoration of structural & functional integrity.
b) Irreversible Cell Injury / Cell Death
if stimulus persists or is severe enough from the start, the cell suffers irreversible cell injury and death.
2 main morphologic patterns: necrosis & apoptosis.
Adaptations are reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment.
Physiologic adaptations are responses of cells to normal stimulation by hormones or endogenous chemical mediators
Pathologic adaptations are responses to stress that allow cells to modulate their structure and function and thus escape injury.
Hypertrophy refers to an increase in the size of cells, that results in an increase in the size of the affected organ
The hypertrophied organ has no new cells, just larger cells.
Types:
a) physiologic b) pathologic
Causes:
a) increased functional demand b) hormonal stimulation
concise lecture with tables and pictures about chronic inflammation, its mediators, mechanism and sequele. Granulomatous inflammation with different types of granulomas along with histopathology pictures and description.
Apoptosis is a controlled, programmed cell death process that is essential for normal development and homeostasis. During apoptosis, cells actively trigger intracellular events that lead to cell fragmentation and phagocytosis without causing inflammation. Apoptosis is distinct from necrosis, which is unregulated cell death caused by external cellular injuries. Key aspects of apoptosis include activation of caspases, DNA fragmentation, and changes to cell membranes that mark cells for phagocytosis. Apoptosis pathways can be triggered by extracellular signals or internal cell damage and are important in development, tissue homeostasis, and diseases like cancer when the process goes awry.
This document discusses potential stem cell sources and treatments for spinal cord injury. It summarizes preclinical studies showing umbilical cord blood cells improve recovery when transplanted shortly after spinal cord injury in rat models. Recent clinical trials have transplanted umbilical cord blood cells into humans with chronic spinal cord injury. The document also discusses that lithium treatment may reinforce regeneration by increasing neurotrophin production and survival of transplanted cells in injured spinal cords. ChinaSCINet is conducting several clinical trials testing lithium and umbilical cord blood cell transplants to treat spinal cord injury.
The document provides an overview of the immune system and inflammation. It discusses the inflammatory response process, including the vascular and cellular stages. It describes the signs of inflammation (rubor, tumor, calor, dolor, functio laesa) and cells involved in inflammation like neutrophils, eosinophils, basophils, and monocytes. It also discusses mediators of inflammation like kinins, complement system, histamine, serotonin, arachidonic acid metabolites, platelet activating factor, cytokines, and nitric oxide. Finally, it covers acute phase response, types of inflammation (acute vs chronic), and factors that influence wound healing.
The document defines and discusses various types of necrosis, or cell death, that can occur in living tissue. It begins by defining necrosis as the localized death of cells or tissue occurring in the living body without chemical message. The document then discusses different mechanisms that can lead to necrosis, including swelling, calcium overload, and free radical damage. It describes various histological changes seen in necrotic cells and tissue at both the light and electron microscopic level. Several types of necrosis are also outlined, such as coagulative, caseous, liquefactive, and gangrenous necrosis. Complications from necrosis and treatments are briefly mentioned at the end.
Acquired immunity involves lymphocytes and develops a slower response to specific microbes. It includes two types: the humoral response which produces antibodies, and the cell-mediated response involving cytotoxic lymphocytes. Memory lymphocytes provide a rapid response upon future exposures to the same antigen. T cells are activated by antigens presented on MHC proteins and perform cytotoxic functions or help coordinate immune responses by activating other cells. B cells are activated by contact with antigens and differentiate into memory B cells or antibody-secreting plasma cells. Antibodies neutralize pathogens or mark them for destruction.
This document summarizes a morning conference case involving a 14-year-old girl with chronic rhinosinusitis and recurrent ear infections. She presented with low immunoglobulin levels, recurrent sinopulmonary infections, and a low number of circulating B cells, consistent with a diagnosis of primary immunodeficiency. Specifically, her condition matches the characteristics of autosomal recessive agammaglobulinemia, which involves a profound loss of all immunoglobulin isotypes. The conference discusses the genetic causes, clinical manifestations, and treatment approach for this form of primary immunodeficiency.
Una breve ma dettagliata review sulle varie fasi di guarigione del tessuto tendineo.
http://www.calzetti-mariucci.it/shop/prodotti/i-tendini-biologia-patologia-aspetti-clinici
Tratto da: I tendini: biologia, patologia, aspetti clinici
Gian Nicola Bisciotti
Ricambi Iveco di carrozzeria: come acquistare ricambi Iveco non originali omologati e certificati per tutelare la sicurezza del veicolo e degli utenti stradali.
Mobilità sostenibile: soddisfare le esigenze di trasporto della generazione attuale senza
impedire alle prossime di fare altrettanto.
L'impegno di Iveco per l'ambiente si concretizza a tutti i livelli del ciclo di vita dei suoi prodotti:
dalla selezione delle materie prime e dei componenti ai metodi di produzione, dalle caratteristiche
e prestazioni dei veicoli alla loro riciclabilità.
La mobilità sostenibile è rispetto per noi e per i nostri figli.
Este documento resume la situación económica mundial en 2015, destacando las recesiones en Brasil, China y México. Brasil se enfrenta a una fuerte desaceleración económica y crisis política. China experimenta una crisis inmobiliaria y problemas para mantener su tipo de cambio. Estados Unidos mantiene su supremacía económica. México se ve afectado por la apreciación del dólar y la caída de los precios del petróleo, con un crecimiento esperado del 2% para 2015.
3 Things Every Sales Team Needs to Be Thinking About in 2017Drift
Thinking about your sales team's goals for 2017? Drift's VP of Sales shares 3 things you can do to improve conversion rates and drive more revenue.
Read the full story on the Drift blog here: http://blog.drift.com/sales-team-tips
Aterosclerosi e danno d’organo: - di P. BuonamicoMedOliveOil
Il danno d’organo: l’aterosclerosi - di P. Buonamico. 5 giugno 2012. Corso di formazione "valore nutrizionale e salutistico di prodotti agroalimentari” - Università degli studi di Bari.
Questo primo Pocket Book affronta un tema di grande attualità: la riabilitazione in seguito a risoluzione chirurgica di un danno condrale. In particolare, al capitolo che introduce le caratteristiche anatomiche della cartilagine, segue un approfondimento sui vari tipi di danno condrale e sui conseguenti tipi di trattamento.
http://www.calzetti-mariucci.it/shop/prodotti/la-cartilagine-linee-guida-dopo-trattamento-chirurgico
A deep presentation of the link between the esophagitis and the esophageal cancer. From the esophagus inflammation (also from the GERD), to a metaplasia (Barrett) to a neoplasia.
41. RIPARAZIONE MIOCARDIO INFARTUATO
Apoptosi (entro 12h)
Morte
cellulare
Necrosi (fino a 4gg)
Esigenza particolare:
riparazione in un tessuto in movimento continuo
Persistenza TGF-β anche per anni
miofibroblasti
42. RIPARAZIONE: CELLULE STAMINALI
Divisione asimmetrica e le nicchie
Cellule ovali nei canali di Hering
- Progenitori epato-biliari -
Wilson et al. Nature Reviews Immunology 6, 93–106 (February 2006)
93–
45. RIPARAZIONE: CONCLUSIONI
-UNA PLETORA DI FATTORI IMPLICATI NELLA RIPARAZIONE
-RIDONDANZA MOLECOLARE/BIOCHIMICA
-COORDINAZIONE CRONOLOGICA CRUCIALE
-PECULIARITA’ TESSUTO-SPECIFICHE
-ELEMENTI COSTANTI IN OGNI PROCESSO RIPARATIVO
-ANALOGIE MOLECOLARI RIPARAZIONE-CRESCITA TUMORALE
46. IL PROCESSO RIPARATIVO:
Letture consigliate
www.pubmed.org
Pontieri “Patologia Generale” Piccin Nuova Libraria S.p.A.
Robbins “Le basi patologiche delle malattie” 7.a Ed. Elsevier Italia