1. The document reviews literature on the relationship between immune system factors and brain development in autism disorder.
2. It finds that pro-inflammatory cytokines like IL-6 have been associated with autism and can impair neural cell adhesion/migration and synapse formation when overexpressed.
3. The timing of immune system disturbances and brain development may provide insights into autism pathogenesis.
Cardiovascular, respiratory, and nervous systems neonatal pathology in premature babies leads to systemic and organ hypoxia, which is one of the main risk factors for premature retinopathy (PR) development. Among the certain neuron-specific proteins, the most studied and adequately characterizing the blood-brain barrier (BBB) proper membrane function is neuro-specific enolase (NSE), which is currently used to diagnose acute conditions characterized by cerebral ischemia and brain hypoxia, occurring with impaired BBB function. by D.I. Tashkhanova and M.Kh. Karimova 2020. The nse predictive value in pr development. International Journal on Integrated Education. 3, 11 (Nov. 2020), 5-7. DOI:https://doi.org/10.31149/ijie.v3i11.813. https://journals.researchparks.org/index.php/IJIE/article/view/813/779 https://journals.researchparks.org/index.php/IJIE/article/view/813
Cardiovascular, respiratory, and nervous systems neonatal pathology in premature babies leads to systemic and organ hypoxia, which is one of the main risk factors for premature retinopathy (PR) development. Among the certain neuron-specific proteins, the most studied and adequately characterizing the blood-brain barrier (BBB) proper membrane function is neuro-specific enolase (NSE), which is currently used to diagnose acute conditions characterized by cerebral ischemia and brain hypoxia, occurring with impaired BBB function. by D.I. Tashkhanova and M.Kh. Karimova 2020. The nse predictive value in pr development. International Journal on Integrated Education. 3, 11 (Nov. 2020), 5-7. DOI:https://doi.org/10.31149/ijie.v3i11.813. https://journals.researchparks.org/index.php/IJIE/article/view/813/779 https://journals.researchparks.org/index.php/IJIE/article/view/813
Pathophysiology of TBI is complex and consists of acute and delayed injury. In the acute phase, brain tissue destroyed upon impact includes neurons, glia, and endothelial cells, the latter of which makes up the blood-brain barrier. In the delayed phase, “toxins” released from damaged cells set off cascades in neighboring cells eventually leading to exacerbation of primary injury. As researches further explore pathophysiology and molecular mechanisms underlying this debilitating condition, numerous potential therapeutic strategies, especially those involving stem cells, are emerging to improve recovery and possibly reverse damage. In addition to elucidating the most recent advances in the understanding of TBI pathophysiology, this review explores two primary pathways currently under investigation and are thought to yield the most viable therapeutic approach for treatment of TBI: manipulation of endogenous neural cell response and administration of exogenous stem cell therapy.
Natural Treatments for ADHD - April 11, 2018Louis Cady, MD
This presentation will be delivered April 11, 2018 on recorded webinar for the Autism Global Conference. It was my pleasure to prepare and present this lecture (in webinar form), outlining a coherent philosophy of finding biological underpinnings that can cause or contribute to, or exacerbate, mental dysfunction. In the case of this presentation, the question is "How much of ADHD symptomatology is caused by a lack of a good medication, or, rather, lack of a coherent strategy for finding and fixing underlying biological abnormalities?"
Those biological abnormalities in this presentation include MTHFR polymorphisms, COMT polymorphisms, elemental deficiencies (lithium, magnesium, zinc, iron, and copper), essential fatty acid deficiencies, the confound of high fructose corn syrup, and many others.
Rational strategies for nutraceutical intervention are reviewed.
Dominic Walsh - A Critical Appraisal of the Pathogenic Protein Spread Hypothe...Alzforum
Presentation made April 8, 2016 at the live webinar hosted by Alzforum - http://www.alzforum.org/webinars/webinar-pathogenic-protein-spread-lets-think-again
This lecture was presented on March 29, 2019 in Rapid Citry, South Dakota, for the conference co-sponsored by the Manlove Psychiatric Group and the Brain Injury Center.
It reviews the uptick in diagnosis of ADHD, the raiontale for its concern, causative factors, and how it can be worked up holistically and in a balanced, not necessarily medication-oriented way.
Use of high dose fish oil, iron supplementation, and how to overrcome nutritional deficiencies are discussed.
The Do It To Yourself Treatment of Depression - Webinar #3Louis Cady, MD
This is the third in a series of five webinars. The first was on staying alive by boosting your immunity during COVID 19. The second was on not screwing yourself up inside your head. This third one encompasses a romp through the peer reviewed medical literature looking for supplements and nutrients that you could use to self treat depression at home, CAREFULLY. Numerous cautions and warnings are included.
The driving impetus to this program is that many people - due to social isolation and their mental health care, or medical practitioners' offices being closed down - have not been able to get help or succeed in optimizing their treatment for depression. There are multiple useful nutrients for both depression and anxiety in nature's abundant pharmacopeia, and this webinar touches on just a few of them.
I hope you enjoy it.
The proteins are so much important, are versatile molecules because can realize diverses functions and we can use it like: enzymes: can catalysis chemical reactions
Hormones: the proteins can work with the plataletes to help to the blood coagulation
Transport of substances
Immunological factor: the antibodies produced with leukocyte
And the most important characteristic, they are molecular target so, we can use it to medical treatment, therapies to the cancer and another diseases . Also we can use the proteins presence and characteristic behavior for diagnosis of many sicknesses
1.Poor protein control key to Alzheimer's progression
New research investigating the pattern of protein build-up in Alzheimer's brains may open the door to a deeper understanding.
Previous research has identified that certain areas of the brain are more sensitive to the aggregation of proteins. The disease often begins in the entorhinal region (at the base of the brain) and spreads out to all of the neocortex (the largest part of the cerebral cortex)
How did it?
They analyzed approximately 500 samples of healthy brain taken from the Allen Brain Atlas In the healthy tissue, they observed a distinctive joint of genes important in the control of beta amyloid and tau protein. They contrasted with Alzheimer`s brains and discovered a identical pattern in advance of the sickness throughout the brain.
2. 2 Zika Virus Proteins Linked to Microcephaly ID'd
First study to examine Zika infection in human neural stem cells from second-trimester fetuses, researchers say.
USC researchers have tracked down two Zika proteins potentially responsible for thousands of microcephaly cases; taking one small step toward preventing Zika-infected mothers from birthing babies with abnormally small heads. Babies with microcephaly have abnormally small heads and brains. The Zika virus include 10 proteins, however only NS4B and NS4A are the responsible, in accordance with the study published in the journal Cell Stem Cell. These malicious proteins, researchers discovered, have two shared life goals: to handicap fetal brain formation and to mobilize their malevolent forces.
Pathophysiology of TBI is complex and consists of acute and delayed injury. In the acute phase, brain tissue destroyed upon impact includes neurons, glia, and endothelial cells, the latter of which makes up the blood-brain barrier. In the delayed phase, “toxins” released from damaged cells set off cascades in neighboring cells eventually leading to exacerbation of primary injury. As researches further explore pathophysiology and molecular mechanisms underlying this debilitating condition, numerous potential therapeutic strategies, especially those involving stem cells, are emerging to improve recovery and possibly reverse damage. In addition to elucidating the most recent advances in the understanding of TBI pathophysiology, this review explores two primary pathways currently under investigation and are thought to yield the most viable therapeutic approach for treatment of TBI: manipulation of endogenous neural cell response and administration of exogenous stem cell therapy.
Natural Treatments for ADHD - April 11, 2018Louis Cady, MD
This presentation will be delivered April 11, 2018 on recorded webinar for the Autism Global Conference. It was my pleasure to prepare and present this lecture (in webinar form), outlining a coherent philosophy of finding biological underpinnings that can cause or contribute to, or exacerbate, mental dysfunction. In the case of this presentation, the question is "How much of ADHD symptomatology is caused by a lack of a good medication, or, rather, lack of a coherent strategy for finding and fixing underlying biological abnormalities?"
Those biological abnormalities in this presentation include MTHFR polymorphisms, COMT polymorphisms, elemental deficiencies (lithium, magnesium, zinc, iron, and copper), essential fatty acid deficiencies, the confound of high fructose corn syrup, and many others.
Rational strategies for nutraceutical intervention are reviewed.
Dominic Walsh - A Critical Appraisal of the Pathogenic Protein Spread Hypothe...Alzforum
Presentation made April 8, 2016 at the live webinar hosted by Alzforum - http://www.alzforum.org/webinars/webinar-pathogenic-protein-spread-lets-think-again
This lecture was presented on March 29, 2019 in Rapid Citry, South Dakota, for the conference co-sponsored by the Manlove Psychiatric Group and the Brain Injury Center.
It reviews the uptick in diagnosis of ADHD, the raiontale for its concern, causative factors, and how it can be worked up holistically and in a balanced, not necessarily medication-oriented way.
Use of high dose fish oil, iron supplementation, and how to overrcome nutritional deficiencies are discussed.
The Do It To Yourself Treatment of Depression - Webinar #3Louis Cady, MD
This is the third in a series of five webinars. The first was on staying alive by boosting your immunity during COVID 19. The second was on not screwing yourself up inside your head. This third one encompasses a romp through the peer reviewed medical literature looking for supplements and nutrients that you could use to self treat depression at home, CAREFULLY. Numerous cautions and warnings are included.
The driving impetus to this program is that many people - due to social isolation and their mental health care, or medical practitioners' offices being closed down - have not been able to get help or succeed in optimizing their treatment for depression. There are multiple useful nutrients for both depression and anxiety in nature's abundant pharmacopeia, and this webinar touches on just a few of them.
I hope you enjoy it.
The proteins are so much important, are versatile molecules because can realize diverses functions and we can use it like: enzymes: can catalysis chemical reactions
Hormones: the proteins can work with the plataletes to help to the blood coagulation
Transport of substances
Immunological factor: the antibodies produced with leukocyte
And the most important characteristic, they are molecular target so, we can use it to medical treatment, therapies to the cancer and another diseases . Also we can use the proteins presence and characteristic behavior for diagnosis of many sicknesses
1.Poor protein control key to Alzheimer's progression
New research investigating the pattern of protein build-up in Alzheimer's brains may open the door to a deeper understanding.
Previous research has identified that certain areas of the brain are more sensitive to the aggregation of proteins. The disease often begins in the entorhinal region (at the base of the brain) and spreads out to all of the neocortex (the largest part of the cerebral cortex)
How did it?
They analyzed approximately 500 samples of healthy brain taken from the Allen Brain Atlas In the healthy tissue, they observed a distinctive joint of genes important in the control of beta amyloid and tau protein. They contrasted with Alzheimer`s brains and discovered a identical pattern in advance of the sickness throughout the brain.
2. 2 Zika Virus Proteins Linked to Microcephaly ID'd
First study to examine Zika infection in human neural stem cells from second-trimester fetuses, researchers say.
USC researchers have tracked down two Zika proteins potentially responsible for thousands of microcephaly cases; taking one small step toward preventing Zika-infected mothers from birthing babies with abnormally small heads. Babies with microcephaly have abnormally small heads and brains. The Zika virus include 10 proteins, however only NS4B and NS4A are the responsible, in accordance with the study published in the journal Cell Stem Cell. These malicious proteins, researchers discovered, have two shared life goals: to handicap fetal brain formation and to mobilize their malevolent forces.
PAGE Running head SCHIZOPHRENIA 1SchizophreniaVernessa.docxkarlhennesey
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Running head: SCHIZOPHRENIA
1
Schizophrenia
Vernessa Combs
PSY350: Physiological Psychology
December 10, 2019
Schizophrenia
The topic selected was schizophrenia. This is a severe and chronic mental disorder affecting the way humans think, feel and behave. Although this mental disorder is not very common, it has disabling symptoms.
Schizophrenia has continuously been viewed as a disorder that occurs in neurodevelopment. It is associated with a microdeletion syndrome of a chromosome. Neurons migrate to the pial surface from the brain's ventricular zone. "Migration of the neuron cell body is mediated via microtubule-based transport organized by the centrosome. First, the centrosome moves up the microtubule, followed by the nucleus and the cell body” (Pearlson, 2015). Neuronal migrations are reportedly caused by Reelin.
The etiology of schizophrenia is unknown, however, several risk factors have been associated with its development. These include environmental and genetic factors. Genetic factors are, however, insufficient to account for the development of the disease. They must be accompanied by other factors for the disease to develop. "Because the concordance rate for monozygotic twins only approaches 50%, genetic makeup alone is not sufficient for the development of schizophrenia, and non-genetic or sporadic forms of the disorder must exist” (Miyamoto et al, 2013).
Environmental factors that play an important role in the etiology of schizophrenia include obstetric complications such as hypoxia, preeclampsia, and premature birth. Other environmental factors include maternal viral infections and stress occurring in neurodevelopment. Stress during neurodevelopment may be caused by other factors such as microbial infections.
The pathology of schizophrenia includes the transcriptional dysregulation at the cerebral cortex and chromosomal conformations. “Anatomic, neurotransmitter and immune system abnormalities have been implicated in the pathophysiology of schizophrenia” (Miyamoto et al, 2013). Differences have been observed in the brains of people with schizophrenia compared to the brains of people without the disease in neuroimaging studies. The medial temporal areas of the brain have a decreased volume while the ventricles are larger. Structural abnormalities such as volume reductions and ventricular enlargements have been associated with the disease.
The dopaminergic system abnormalities are also associated with schizophrenia. The immune system is also disturbed in people with the disease. “Overactivation of the immune system (eg, from prenatal infection or postnatal stress) may result in overexpression of inflammatory cytokines and subsequent alteration of brain structure and function” (Nuckols et al, 2013). Anatomic abnormalities may also be observed in the hippocampus.
In the prefrontal cortex, there has been a reported increase in neuronal density. One of the areas of the prefrontal cortex, area 9, has been found to h ...
Epilepsy is a chronic neurological disorder which is caused by various factors which may vary according to the age of patients which results in asynchronization of neurons. Cognitive functional impairment is mostly seen in epileptic patients compared to the general population, and the degree of its impairment varies from one another according to the epilepsy syndrome. Behavioral changes are more seen in epileptic people and people with drug-resistant epilepsy, frequent seizures, and associated neurological or mental abnormalities. In children and adults, many data suggest a correlation between behavior/cognition and some other specific epilepsy syndromes. The major predictors of such behavioral changes in children with epilepsy are epilepsy itself, treatment, the underlying structural lesion, and epilepsy treatment.
Dr. Lucija Tomljenovic, The biological basis for the neurotoxicity of vaccinesJack Olmsted
Dr. Lucija Tomljenovic is an early career postdoctoral fellow. She was awarded a PhD in 2009 in Biochemistry, from the Comparative Genomics Centre at James Cook University in Townsville, Australia. In 2010, she joined the Neural Dynamics Research Group at the University of British Columbia (Chris Shaw’s lab) and is currently researching the neurotoxic effects of aluminum vaccine adjuvants. Tomljenovic has recently become an Associate Editor of the Journal of Alzheimer’s Disease. She values open-minded discussions on controversial topics and the pursuit of truth in research endeavors, wherever they may lead.
Panel:
Kathleen Hallal, GMO Free News Host
Rachel Linden, GMO Free News Co-Host
Zoey O'Toole, Thinking Moms Revolution
Dr. Lucija Tomljenovic
Jack Olmsted, Producer
Dr. Mercola Interview with Dr. Tomljenovic: How Vaccine Adjuvants Affect Your Brain
http://articles.mercola.com/sites/articles/archive/2015/03/29/vaccine-adjuvants-brain-effects.aspx
HPV Vaccine Safety and Efficacy Issues: Dr. Tomljenovic's in Vancouver, 2015.
https://www.youtube.com/watch?v=9Uu3iWA1UWw
Question List:
Dr. Tomljenovic: Regarding the questions, if there are no comments it means I will answer these questions during the show:
Which vaccines cause the antibodies to attack the brain?
Are some vaccines/adjuvants more prone to do this? Why or why not?
Comment:That is the million dollar question that no one knows the answer to because this issue has not been studied well enough. Even the pharma admits that they do not know exactly how the adjuvants work. I can give some quotes from the pharma experts.
Just wanted to let you know that I cannot answer this question any better than this.
Did you test OTHER body tissues, or just the brain?
Why would the phenomenon of mimicry only work on the brain tissue?
Comment: It does not work only on brain tissue, it can work on any tissue where there is mimicry between the antigen of the virus/bacteria and that of the host
Have you tried immunizing mice at reduced rates (fewer boosters, like they do in Scandanavian countries) and if so, do they have much fewer issues with autoimmunity?
Comment: We have not immunized the mice (we did not inject them with vaccines), we have only given the mice aluminum in the amounts equivalent to that given to children via vaccinations in the US and Scandinavia. At the time we did this study, we did not look for any autoimmune markers, only behavioral outcomes as well as gene expression in the brains of these mice. In both parameters there were abnormal changes (i.e. abnormal behavior and increased expression of certain pro-inflammatory genes in the brain as well as reduced expression of AChE = acetylcholinesterase which has anti-depression/anxiety effect. Low AChE activity is associated with deficits in neurodevelopment)
The question of how we live longer—and why only a minority of humans have good health and a long life—has confused people for millennia. Over the past few decades, we have learned that human lifespan is determined by both the genes and external influences, and that these factors act, by means of numerous genetic pathways, to regulate the cellular and systemic processes that ultimately cause aging and death.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
2. How to cite this article: Luisetto M, Ahmed Y R, Behzad Ni, Farhan A K, Ghulam R M. Immune Shock -Chronologic Event in Some Brain Pathology.
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From Reference : we have find that
According Wei H et al. [1] “the mechanisms responsible of
autism pathogenesis are not understood, studies have suggested
that localized inflammation of the CNS may contribute to the
development of autism. Recent evidence shows that IL-6 has a
crucial role in the development and plasticity of CNS.
Autistic brain disorder is the most severe groups of neuro-
developmental disorders, referred to ASDs, with problems in
communication, social skills, and repetitive kind of behavior.
Susceptibility to autism is clearly attributable to genetic factors
[1-4], but the etiology of the disorder is unknown. Recent
studies suggest that a combination of environmental risk factors,
autoimmune conditions and localized inflammation of the central
nervous system may contribute to the pathogenesis of autism.
Interleukin (IL)-6 was originally found to be a major inducer
of immune and inflammatory response. Recent studies and points
to a crucial role of IL-6 within CNS.In the CNS IL-6 can trigger
the cell responses mediating inflammation responses, neuro-
genesis, glio-genesis, and cell growth, cell survival, myelination
and demyelination. IL-6 is normally expressed at relatively low
levels in the brain. However, in the presence of brain injury or
inflammation, IL-6 is elevated in the cerebral spinal fluid and
brain homogenates. Chronic over-expression of IL-6 in transgenic
mice causes neuroanatomical and neurophysiological alterations
associated with neurological disease. IL-6 and leukaemia inhibitory
factor were found to promote astrocytic differentiation of neural
stem⁄progenitor cells. Most recently, Oh et al demonstrated that
IL-6 promotes specific neuronal differentiation of neural progenitor
cells from the adult hippocampus.
Recent studies have reported an association of cytokines with
autism. TNF-α, IFN-γ, IL-1β and IL-12 were found to be elevated in
blood mononuclear cells, serum and plasma from autistic subjects.
Employing a cytokine PCR array, Vargas et al demonstrated that
IL-6, TNFα, transforming growth factor (TGF)-β1 and macrophage
chemo-attractant protein (MCP)-1 were increased in autistic brains.
In addition, MCP-1, IL-8 and other proinflammatory molecules were
also found to be significantly elevated in the cerebrospinal fluid of
autistic children. Consistent with the these findings, our studies
using a multiple bead immunoassay showed that IL-6, TNFα, IL-8,
GM-CSF and IFNγ were significantly increased in the fontal cortices
of autistic subjects as compared with the age-matched controls [5].
All these findings suggest that the immune system and
cytokines may play important roles in the pathogenesis of autism.
However, the mechanisms by which immune dysfunction and
cytokine alteration contribute to the pathogenesis of autism remain
unknown. In this study, we examined IL-6 in the cerebellum of
autistic subjects. Our results: that IL-6 was significantly increased
in the cerebellum of autistic patients as compared to controls. In
addition, we over-expressed IL-6 in cerebral granule utilizing a
viral construct expression approach to study the effects of IL-6 on
neural cell properties and synapse formation. Was demonstrated
that IL-6 over-expression in granule cells caused an impairment in
adhesion and migration properties. However IL-6 over-expression
stimulated the formation of granule cell excitatory synapses,
while having no effect on inhibitory synapses. This results provide
evidence for an association of aberrant IL-6 expression with autism
disorder. Impaired neural cell adhesion and migration, as well as the
excessive formation of excitatory synapses caused by elevated IL-6
expression could be an underlying cellular mechanism partially
responsible for the pathogenesis of autism.
This study demonstrates that IL-6 was significantly increased
in the cerebellum of autistic patients as compared controls. And
IL-6 over-expression in cerebellar granule cells in vitro impaired
granule cell adhesion and migration properties. In addition, we
found that IL-6 over-expression stimulated the formation of
excitatory synapses of granule cells, while having no effect on the
inhibitory synapses. These findings suggest that the elevated IL-6
in the autistic brain could cause an imbalance of neuronal circuits
through its effects on neural cell adhesion/migration and synapse
formation, and contribute to the development of autism”[1].
Hu s et al. [2] written that “Cytokines induce neuronal injury via
the free radical nitric oxide; the precise mechanism is unclear. We
investigated the hypothesis that cytokine-mediated neurotoxicity
in primary cultures of human fetal neurons occurs via an apoptotic
mechanism triggered by NO. Treatment of mixed neuronal/glial cell
in vitro cultures with IFN-gamma plus interleukin (IL)-1 beta for
13 days induced a high output of NO accompanied by neuronal cell
loss. The NO synthase inhibitor N-monomethyl-L-arginine (NMMA)
significantly attenuated cytokine-induced neuronal loss, confirming
the involvement of NO. Cytokine-mediated neuronal cell damage-
injury caused morphologic changes and a DNA fragmentation
pattern: apoptosis. These findings could lead to the development
of new therapies for neuro degenerative diseases involving glia,
cytokines, and NO” [2].
Grunnet LG et al. [3] showed, “Proinflammatory cytokines are
cytotoxic to beta-cells and have been implicated in the pathogenesis
of type 1diabetes and islet graft failure. The intrinsic properties
in mitochondrial apoptotic pathway in cytokine-induced beta-cell
death is unclear. Here, cytokine activation of the intrinsic apoptotic
pathway and the role of the two proapoptotic Bcl-2 proteins, Bad
and Bax, were examined in beta-cells.
HumanisletsandINS-1cellswereexposedtoapro-inflammatory
cytokines (interleukin-1beta, IFN-gamma, and/or TNF-alpha).
Activation of Bad was determined by Ser136 dephosphorylation,
mitochondrial stress by changes in mitochondrial metabolic
activity and cytochrome c release, downstream apoptotic signaling
by activation of caspase-9 and -3, and DNA fragmentation.
We found that proinflammatory cytokines induced calcineurin-
dependent dephosphorylation of Bad Ser136, mitochondrial stress,
cytochrome c release, activation of caspase-9 and -3, and DNA
fragmentation. Inhibition of Bad Ser 136 dephosphorylation or Bax
inhibit cytokine-induced intrinsic pro-apoptotic signaling.
3. How to cite this article: Luisetto M, Ahmed Y R, Behzad Ni, Farhan A K, Ghulam R M. Immune Shock -Chronologic Event in Some Brain Pathology.
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Our findings demonstrate that the intrinsic mitochondrial
apoptotic pathway contributes significantly to cytokine-induced
beta-celldeathandsuggestafunctionalroleofcalcineurin-mediated
Bad Ser136 dephosphorylation and Bax activity in cytokine-
induced apoptosis” [3]. From website http://www.autism-society.
org/what-is/causes/
“it is accepted that it is caused by abnormalities in brain
structure or functionality . Brain scans show differences in the
shape and structure of the brain in children with autism compared
to in neurotypical children. In many families, there appears to be
a pattern of autism or related disabilities, further supporting the
theory that the disorder has a genetic basis. While no one gene
has been identified as causing agent, researchers are searching for
irregular segments of genetic code that children with autism may
have inherited. It also appears that some children are born with a
susceptibility to autism, but researchers have not yet identified a
single “trigger” that causes autism to develop.
Other researchers are investigating the possibility that under
certain conditions, a cluster of unstable genes may interfere with
brain development, resulting in autism. Still other researchers are
investigating problems during pregnancy or delivery as well as
environmentalfactorssuchasviralinfections,metabolicimbalances
and exposure to chemicals.
Genetic Vulnerability
Some harmful substances ingested during pregnancy also have
been associated with an increased risk of autism.”
Watts TJ [4] showed that “Autism is well known as a complex
developmental brain disorder with a uncertain pathogenesis. The
definitive mechanisms that promote autism are poorly understood
and mostly unknown, yet available theories do appear to focus on
the disruption of normal cerebral development and its subsequent
implications on the functional brain unit. The main conclusion is
that although there is not a clear pathway of mechanisms directed
towards a simple pathogenesis and an established link to autism
on the symptomatic level; there are however several important
theories (neural connectivity, neural migration, excitatory-
inhibitory neural activity, dendritic morphology, neuroimmune;
calcium signalling and mirror neurone) which appear to offer an
explanationtohowautismdevelops.Itseemsprobablethatautism’s
neurodevelopmental defect is ‘multi-domain’ in origin (rather
than a single anomaly) and is hence distributed across numerous
levels of study (genetic, immunopathogenic, etc.). A more definitive
understanding of the pathogenesis could facilitate the development
of better treatments for this complex psychiatric disorder.
Neuroimaging has been playing a crucial role in studying autism
spectrum disorders (ASD). Among them, Functional Magnetic
Resonance Imaging (fMRI) is remarkably noted. fMRI has an
important role in understanding neurobiologic basis for autism and
autism-spectrum disorders. As a normal and autism affected brain
do not have significant size differences, functional neuroimaging
modalities are greatly aiding to investigate the functional activation
to probe the functional dysfunction of an autism affected brain.
Besides, fMRI findings are providing ASD patho-physiologic
informations and trying to find the etiology of autism to develop
rationally derived and targeted treatments. According to Gabriel S.
Ditcher though the findings have considerable heterogeneity but
the common are [2]:
a. Hypoactivation in nodes of the “social brain” during social
processing tasks, including regions within the prefrontal cortex, the
posterior superior temporal sulcus, the amygdala, and the fusiform
gyrus;
b. Aberrant frontostriatal activation during cognitive control
tasks works relevant to restricted and repetitive behaviors and
interests, including regions within the dorsal prefrontal cortex and
the basal ganglia;
c. Differential lateralization and activation of language
processing and production regions during communication tasks;
d. Anomalous mesolimbic responses to social and nonsocial
rewards;
e. Task-based long-range functional hypoconnectivity and
short-range hyper-connectivity; and
f. Decreased anterior-posterior functional connectivity during
resting states.
Recent efforts of neuropsychiatric genetics are being exerted
to reveal genetic mechanism or biological pathways underlying
autism. All developmental trajectories for brain growth are seen
in autism, suggesting considerable heterogeneity in the specific
underlying genetic mechanisms affected. About 20 mostly rare
genes or gene mutations are discovered that are each involved in a
molecular aspect of the development of neuronal connections, the
fMRI and genetic findings in autism closed a loop that validated a
developmental neurobiological based model of autism. fMRI studies
are focusing on further articulation of functional connectivity
disturbances, the neural bases of deficits and skills, and the
disturbances in higher levels of brain organization related to control
and regulation of thinking, feeling, and behaving [5].
According Minshew NJ et al. [5] “Functional magnetic resonance
imaging studies have had a profound impact on the delineation of
the neurobiologic basis for autism. Discovery in fMRI technology for
investigating connectivity, resting state connectivity, and a default
mode network have provided further detail about disturbances in
brain organization -behavior relationships in autism disorder.
Recent fMRI studies have provided evidence of enhanced
activation and connectivity of posterior, or parietal-occipital,
networks and enhanced reliance on visuospatial abilities for
visual and verbal reasoning in high functioning individuals with
autism. Evidence indicates the altered activation in front to-striatal
networks related to cognitive control, involving anterior cingulate
4. How to cite this article: Luisetto M, Ahmed Y R, Behzad Ni, Farhan A K, Ghulam R M. Immune Shock -Chronologic Event in Some Brain Pathology.
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cortex, and altered connectivity in the other resting state and the
default mode network. The findings suggest that the specialization
of many cortical networks of the human brain has failed to develop
fully in high functioning individuals with autism.
This work provides a specification about neurobiologic basis
for this brain syndrome and for the co-occurrence of the signs
and symptoms as a syndrome. With this knowledge has come new
neurobiologically based opportunities for intervention“[6].
Gabriel DS [6] written:“ASDS :, common themes have emerged,
including: (i) hypoactivation in nodes of the “social brain” during
social processing tasks, including regions within the prefrontal
cortex, the posterior superior temporal sulcus, the amygdala, and
thefusiformgyrus;(ii)aberrantfrontostriatalactivationINcognitive
control tasks relevant to restricted and repetitive kind behaviors
and interests, including regions within the dorsal prefrontal cortex
andthebasalganglia;(iii)differentiallateralizationandactivationof
language processing and production regions during communication
tasks; (iv) anomalous mesolimbic responses to social and nonsocial
rewards; (v) task-based long-range functional hypoconnectivity
and short-range hyper-connectivity; and (vi) decreased anterior-
posterior functional connectivity during resting states [7].”
Polšek D et al. [7] “Autism spectrum disorders (ASD)
represent complex neurodevelopmental disorders characterized
by impairments in reciprocal social interactions, abnormal
development and use of language, and monotonously repetitive
behaviors. With an estimated heritability of more than 90%, it is
the most strongly genetically influenced psychiatric disorder of
the young age. In spite of the complexity of this disorder, there
has recently been much progress in the research on etiology,
early diagnosing, and therapy of autism. . This review provides a
comprehensive summary of morphological and neurochemical
alterations in autism known to date. Finally, we mention the
progress in establishing new standardized diagnostic measures and
its importance in early recognition and treatment of ASD” [8].
Blatt GJ et al. [9] “Autism is defined neurodevelopmental
disorder that affects over 1% of new births in the USA, about 2% of
boys. The etiologies are unknown and they are genetically complex.
There may be epigenetic effects, environmental influences, and
other factors that contribute to the mechanisms and affected neural
pathway(s). Involved brain specific areas in the cerebellum, limbic
system, and cortex. Part(s) of structures appear to be affected
most rather than the entire structure, for example, select nuclei of
the amygdala, the fusiform face area, and so forth. Altered cortical
organization, frequent and narrower minicolumns and early
overgrowth of the frontal portion of the brain, affects connectivity.
Abnormalities include cytoarchitectonic laminar differences, excess
white matter neurons, decreased numbers of GABAergic cerebellar
Purkinje cells, and other events that can be traced developmentally
andcauseanomaliesincircuitry.Problemsinneurotransmissionare
evident according recent receptor / binding site studies especially
in the inhibitory GABA system transmission likely contributing to
an imbalance of the system of excitatory/inhibitory transmission.
As postmortem findings are related to core behavior symptoms,
and technology improves, researchers are gaining a much better
perspective of contributing factors to the disorder” [9].
Brkanac Z et al. [10] “Autism has the highest estimated
heritability (>90%) among behaviorally defined neuropsychiatric
disorders. Rapidly advancing genomic technologies and large
international collaborations have increased our understanding
of the molecular genetic causes of autism. Pharmacogenomic
approaches are currently being applied in two single-gene
disorders, fragile X syndrome and Rett syndrome, which capture
many aspects of the autistic phenotype. This review describes the
current information state of the genetics of autism disorder “[10].
Samsam M et al. [11] “Autism spectrum disorders (ASD)
comprise a group of neurodevelopmental abnormalities that begin
in early childhood and are characterized by impairment of social
communication and behavioral problems including restricted
interests and repetitive behaviors. Several genes have been
implicated in the pathogenesis of ASD, most of them are involved in
neuronal synaptogenesis. A number of environmental factors and
associated conditions such as gastrointestinal (GI) abnormalities
and immune imbalance have been linked to the pathophysiology of
ASD. Although there is a strong genetic base for the disease, several
associatedfactorscouldhaveadirectlinktothepathogenesisofASD
or act as modifiers of the genes thus aggravating the initial problem.
Many children affected with ASD have GI problems as abdominal
pain, chronic diarrhea, vomiting, constipation, G-esophageal
reflux, and intestinal infections. GI tract has a direct connection
with the immune system and an imbalanced immune response is
usually seen in ASD children. Maternal infection or autoimmune
diseases have been suspected. Activation of the immune system
during early development may have deleterious effect on various
organs including the nervous system. In this review paper we have
revisited briefly the GI and immune system abnormalities and
neuropeptide imbalance and their role in the pathophysiology of
ASD and discussed some future research directions” [11].
According Ziats MN et al. [12] “In the September 2012 issue of
The Cerebellum, Fatemi et al. presented an analysis of the role of
the cerebellum in autism. While this is an important work, which
synthesizes the main findings of cerebellar research in autism
spectrum disorders (ASD), we believe there is an alternative
hypothesis to the role of the cerebellum in autism.
The conclusion that the cerebellum is pathogenic in ASD is
predicated on the notion that the cerebellum functions in the
cognitive processes disrupted in autism, although such pathways
remain undiscovered. While the cerebellar contribution to higher
cognition has been debated for decades, a clear mechanistic
understanding of how the cerebellum may integrate with processes
affected in autism, such as theory of mind, is not well established-as
Fatemi et al. noted. Human studies that have consistently implicated
the cerebellum in ASDdo so mostly on the basis of volumetric
imaging studies, or postmortem histologic and molecular changes,
including our own work [3]. However, as opposed to the notion
5. How to cite this article: Luisetto M, Ahmed Y R, Behzad Ni, Farhan A K, Ghulam R M. Immune Shock -Chronologic Event in Some Brain Pathology.
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that these changes are pathogenic-which would require an as yet
undiscovered mechanism for the cerebellum in the higher cognitive
functions affected in ASD-we propose instead that the unique
anatomy, physiology, and development of the cerebellum may
result in an exaggerated manifestation of the brain-wide pathologic
changes that underlie autism, without being causal for the clinical
phenotype. In this sense, then, the cerebellum in autism may be
acting as an “anatomical beacon” of more subtle changes in other
brain regions where the functional pathology actually rests.
The unique anatomy, physiology, and development of the
cerebellummakeitadistinctpartofthehumanbrain.Thecerebellum
has the highest cell density of any brain area, approximately four
times that of the neocortex, and cerebellar Purkinje cells have
more synapses than any other cell type by orders of magnitude.
As building synapses requires the appropriate molecular “toolkit,”
the cerebellum’s molecular complexity of transcripts and proteins
rivals that of the cerebral cortex. Underlying the heightened
synaptogenesis of the cerebellum is the need for energy to carry
out this process, resulting in oxidative metabolic demand that is
similar to the cerebral cortex as well. The implications of these
well-recognized cerebellar properties to autism are profound. The
ASD phenotype is considered to ultimately result from synaptic
dysfunction, which derives from underlying genetic changes that
manifest in aberrant RNA and protein production . Additionally,
autism has a strong and growing association with related problems
in oxidative metabolism. Is it possible that cerebellar pathology
in ASD is more evident than other brain areas purely because the
cerebellum contains more of the components that are disrupted in
autism?
If the molecular and cellular processes that are abnormal in ASD
are dysfunctional throughout the brain, then these observations
suggest that the cerebellum may have properties that result in an
exaggerated manifestation of ASD pathology compared to other
brain regions. Therefore, we hypothesize that the cerebellum
may not be etiological in the pathogenesis of autism spectrum
disorders; rather its unique anatomic and physiologic properties
may accentuate the mechanisms that are aberrant throughout the
autistic brain. Consequently, investigations into autism pathology
may be more readily observed in the cerebellum because the
changes are more obvious than the concomitant changes in other
brain areas responsible for the clinical phenotype.
This hypothesis does not diminish the potential importance of
the cerebellum to autism research. Harnessing this unique property
has serious implications in diagnostic testing, for example with
neuroimaging. Diagnostic tests may be able to identify biological
changes in ASD patients earlier in life, which is known to correlate
with improved patient outcomes, by focusing on the cerebellum.
While cerebellar changes may not directly cause the cognitive
deficits of ASD, they could serve as an “internal biomarker” for the
more subtle alterations that must therefore be ongoing in other
brain areas but would require more sensitive techniques to detect.
Until it is understood how the cerebellum functions in the
higher cognitive processes that are abnormal in autism, the field
must consider the alternative hypothesis that changes found in the
cerebellum of autistic patients are not pathogenic, but rather are
collateral manifestations of the cellular and molecular deficits that
are present throughout the autistic brain. The distinctive nature
of the cerebellum may exaggerate changes that are more subtle
in other brain areas, without being causal of the ASD phenotype.
However, such an interpretation does not diminish the importance
of cerebellar research in autism, as this unique characteristic may
make the cerebellum an ideal diagnostic target [12].”
Schumann CM et al. [13] “The amygdala is one of several
brain regions suspected to be pathological in autism. Previously,
we found that young children with autism have a larger amygdala
than typically developing children. Past qualitative observations
of the autistic brain suggest increased cell density in some nuclei
of the postmortem autistic amygdala. In this first, quantitative
stereological study of the autistic brain, we counted and measured
neurons in several amygdala subdivisions of 9 autism male brains
and 10 age-matched male control brains. Cases with comorbid
seizure disorder were excluded from the study. The amygdaloid
complex was outlined on coronal sections then partitioned into
five reliably defined subdivisions: (1) lateral nucleus, (2) basal
nucleus, (3) accessory basal nucleus, (4) central nucleus, and (5)
remaining nuclei. There is no difference in overall volume of the
amygdala or in individual subdivisions. There are also no changes
in cell size. However, there are significantly fewer neurons in the
autistic amygdala overall and in its lateral nucleus. In conjunction
with the findings from previous magnetic resonance imaging
studies, the autistic amygdala appears to undergo an abnormal
pattern of postnatal development that includes early enlargement
and ultimately a reduced number of neurons. It will be important to
determine in future studies whether neuron loss in the amygdala is
a consistent characteristic of autism and whether cell loss occurs in
other brain regions as well.”
Results
From literature we have find that autism disorder are involved
in young patient , that we have abnormalities (imaging, histology)
in some brain areas, and a complessimpthomatology. Genetic
and environment can produce some unbalances in brain growth
and immunitary situation is involved. Apoptotic signal contribute
in brain growth and immunologic shock can unbalance the
environment producing abnormalities.
Conclusion
In this kind of disorder we have see imaging and histologic
abnormalities related to specific brain areas
involved in a characteristics into matology, produced often
during brain development and not in elder people. Related to some
genetic–immunologic status we can think that immunologick shock
with immune umbalances can produce a abnormal or alterated
micro-environment. Apoptosis is involved in brain growth and
influenced by immunologic status. Even if this pathology has been
6. How to cite this article: Luisetto M, Ahmed Y R, Behzad Ni, Farhan A K, Ghulam R M. Immune Shock -Chronologic Event in Some Brain Pathology.
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deeply studied by many researcher we think are relevant: the time
of expression, micro-environment, immunologic status and genetic
profile.
Discussion
Starting from the evidence that autisms are not elder typical
pathologyandobservingfromtoxicologyandembryologydiscipline
we know that the time is relevant in order to predict some kind of
Congenic pathologies. We have see that in embryology are relevant
genetic informations, the time, micro-environment factors and their
specific time relationship.
From toxicology science we know that some toxic subtancies
produce specific toxicity related the contact time in embiologic-
fetal life whit minor or major physio-anactomic damage. Many
factors are involved as cellular mediators and intercellular signals
but also environmental factors that can modify heavily the normal
neuronal growth and development or connectivity. We have see
from literature a relationship between immunologic status and
some brain condition and that in autism we have a reduced neuron-
connections and population in some area.
Immunologyisinvolvedinapoptosisprocessandaimmunologic
shock in some periods of growth can produce Brain abnormality in
some area (involved in example in relationship behavior or other
inabilities).
We have see “The role of IL-6 within CNS development, IL-6 can
triggerthecellresponsesmediatinginflammationresponses,neuro-
genesis, glio-genesis, and cell growth, cell survival, myelination and
demyelination.”
And Vargas et al demonstrated that IL-6, TNFα, transforming
growth factor (TGF)-β1 and macrophage chemo-attractant protein
(MCP)-1 were increased in autistic brains. IL-6 over-expression in
cerebellar granule cells in vitro impaired granule cell adhesion and
migration properties.
We know that this interleukine is involved in acute flogosis and
can act as b- cell activator. And as TNF is related to fever phenomena
(fever centre in in brain). So what is the effect of an immunologic
shock with b cell stimulation or other immune acute modifications?
Immune imbalances? In neuron apoptosis? Neuroconnectivity?
And related to determinate phenotype? We have see that
“Autism has the highest estimated heritability (>90%) among
behaviorally defined neuropsychiatric disorders” and that “Several
genes have been implicated in the pathogenesis of ASD, most of
them are involved in neuronal synaptogenesis.” We think that in this
kind of pathology must be take in great consideration the timing
in evolution of the physio- anatomic modify related to the micro-
environment modification in a determinate genetic profile.
Clarification
This work is not for diagnostic or therapy intent but only to
produce research hypothesis.
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7. How to cite this article: Luisetto M, Ahmed Y R, Behzad Ni, Farhan A K, Ghulam R M. Immune Shock -Chronologic Event in Some Brain Pathology.
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