Bee venom contain many components like bee venom phospholipase A2 and apamin etc
bee venom phospholipase A2 decrease the neuroinflammation in parkinson's disease helpful to treat PD.
Bee venom contain many components like bee venom phospholipase A2 and apamin etc
bee venom phospholipase A2 decrease the neuroinflammation in parkinson's disease helpful to treat PD.
This presentation mainly deals with Rdna, its properties, sources and applications.According to my opinion the best ppt i have ever prepared to crack the seminar exam during my college days.I am sure everyone is going to like it and please comment if u all like it....
Kinsenoside isolated from Anoectochilus formosanus suppresses LPS-Stimulated ...Cây thuốc Việt
In the present study, we reported that kinsenoside, a major component of Anoectochilus formosanus, inhibited inflammatory reactions in mouse peritoneal lavage macrophages and protects mice from endotoxin shock. In LPSstimulated mouse peritoneal lavage macrophages, kinsenoside inhibited the inflammatory mediators, such as nitric oxide, TNF-!, IL-1", monocyte chemoattractant protein 1, and macrophage migration inhibitory factor production. Furthermore, kinsenoside decreased the formation of a nuclear factor .BYDNA complex and nuclear p65 and p50 protein levels. Kinsenoside inhibited nuclear factor .B translocation through both I.B!-dependent and -independent pathway. In contrast, it stimulated anti-inflammatory cytokine IL-10 generation and enhanced the mRNA expression of IL-10 and suppressor of cytokine signaling 3 in the same cells induced by LPS. In an animal model, both pretreatment and posttreatment of kinsenoside increased the survival rate of ICR mice challenged by LPS (80 mg/kg, i.p.). Pretreatment with kinsenoside decreased serum levels of TNF-!, IL-1", IL-10, monocyte chemoattractant protein 1, and migration inhibitory factor at 1 h after sublethal dose of LPS (40 mg/kg, i.p.) in mice. In contrast, kinsenoside enhanced serum IL-10 level at 24 h after LPS injection in mice. In conclusion, kinsenoside inhibited the production of inflammatory mediators and enhanced antiinflammatory cytokine generation. Therefore, kinsenoside can alleviate acute inflammatory hazards.
Commercial Application of Anoectochilus formosanus: Immunomodulating ActivitiesCây thuốc Việt
Anoectochilus formosanus is an important ethnomedicinal plant of Taiwan. We investigated the effect of oral administration of A. formosanus effective fraction (AFEF) on the innate immune response in mice. Male BALB/c mice were treated orally for 2 weeks with 500, 1000 and 1500 mg/kg of AFEF. Primary peritoneal macrophage harvest from mice that administered with AFEF (500 –1500 mg/kg) was directed to activate phagocytosis. AFEF significantly increased interferon-production from lymph node cells by ConA stimulation for 48 hours in AFEF (1500 mg/kg) treated group. AFEF might be the active fraction in activation of innate immunity.
This presentation mainly deals with Rdna, its properties, sources and applications.According to my opinion the best ppt i have ever prepared to crack the seminar exam during my college days.I am sure everyone is going to like it and please comment if u all like it....
Kinsenoside isolated from Anoectochilus formosanus suppresses LPS-Stimulated ...Cây thuốc Việt
In the present study, we reported that kinsenoside, a major component of Anoectochilus formosanus, inhibited inflammatory reactions in mouse peritoneal lavage macrophages and protects mice from endotoxin shock. In LPSstimulated mouse peritoneal lavage macrophages, kinsenoside inhibited the inflammatory mediators, such as nitric oxide, TNF-!, IL-1", monocyte chemoattractant protein 1, and macrophage migration inhibitory factor production. Furthermore, kinsenoside decreased the formation of a nuclear factor .BYDNA complex and nuclear p65 and p50 protein levels. Kinsenoside inhibited nuclear factor .B translocation through both I.B!-dependent and -independent pathway. In contrast, it stimulated anti-inflammatory cytokine IL-10 generation and enhanced the mRNA expression of IL-10 and suppressor of cytokine signaling 3 in the same cells induced by LPS. In an animal model, both pretreatment and posttreatment of kinsenoside increased the survival rate of ICR mice challenged by LPS (80 mg/kg, i.p.). Pretreatment with kinsenoside decreased serum levels of TNF-!, IL-1", IL-10, monocyte chemoattractant protein 1, and migration inhibitory factor at 1 h after sublethal dose of LPS (40 mg/kg, i.p.) in mice. In contrast, kinsenoside enhanced serum IL-10 level at 24 h after LPS injection in mice. In conclusion, kinsenoside inhibited the production of inflammatory mediators and enhanced antiinflammatory cytokine generation. Therefore, kinsenoside can alleviate acute inflammatory hazards.
Commercial Application of Anoectochilus formosanus: Immunomodulating ActivitiesCây thuốc Việt
Anoectochilus formosanus is an important ethnomedicinal plant of Taiwan. We investigated the effect of oral administration of A. formosanus effective fraction (AFEF) on the innate immune response in mice. Male BALB/c mice were treated orally for 2 weeks with 500, 1000 and 1500 mg/kg of AFEF. Primary peritoneal macrophage harvest from mice that administered with AFEF (500 –1500 mg/kg) was directed to activate phagocytosis. AFEF significantly increased interferon-production from lymph node cells by ConA stimulation for 48 hours in AFEF (1500 mg/kg) treated group. AFEF might be the active fraction in activation of innate immunity.
The current slide focuses on different screening models for neurodegenerative diseases along with a brief description of the diseases where the slides are to the points and brief with detailed evaluation.
IN-VIVO SCREENING METHODS FOR NEURODEGENERATIVE DISEASE.pptxGautamSosa
Neurodegenerative diseases are conditions where nerve cells in the brain and peripheral nervous system gradually degenerate and die, leading to cognitive decline, movement disorders, and sometimes death. Examples include Alzheimer's, Parkinson's, multiple sclerosis and Huntington's disease. Treatment focuses on symptom management, as there are currently no cures for these conditions. Efficacy evaluation of any drug for Alzheimer's, Parkinson's, and multiple sclerosis in in-vivo animal studies, first step is to learn the in-vivo screening model of particular disease.
Chandrayaan-2 mission is a highly complex mission, which represents a significant technological leap compared to the previous missions of ISRO, which brought together an Orbiter, Lander and Rover with the goal of exploring south pole of the Moon. (Presented by SUBHAM PREETAM)
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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 Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
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Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Thyroid Gland- Gross Anatomy by Dr. Rabia Inam Gandapore.pptx
IMMUNOPATHOLOGY ON SLEEPING SICKNESS:
1. Centre for Biotechnology
Siksha ‘O’ Anusandhan
( Deemed to be University )
NAME- SWATI PANDA
REGD NO-1861621056
Designed by- SUBHAM PREETAM
1
2. Immunopathology of Trypanosoma brucei in the central
nervous system (CNS) was studied in infected mice with T.b
brucei were treated with dose of diaminazine aceturate
several times.
Brains were examined using PCR to detect MRNA (cytokine).
The infected & treated animals developed severe chronic
meningo-encephalitis characterized by inflammatory cells &
astrocyte proliferation.
2
3. African sleeping sickness is caused by Trypanozoon species,
extracellular protozoan parasites transmitted by the bite of
tsetse fly.
Many of the clinical symptoms or disease arise as a
consequence of invasion of the central nervous system (CNS)
by the parasite.
The pathological changes associated with this post-treatment
reactions in humans includes severe meningitis, perivascular
cuffing, encephalitis, astrocyte activation.
The resulting inflammatory lesions in the CNS are composed
mostly of plasma cells, macrophages, activated T cell.
3
4. Recent work has pointed the production of cytokines by glial
cells within the brains of infected individuals may give rise to
the symptoms of late stage sleeping sickness & be important
in generating the inflammatory changes seen in the CNS.
The current work was undertaken to identify which cytokines
may be involved in the pathogenesis of the post-treatment
reactions.
4
5. Female CD-1 Inoculated with 2*10⁴ T.b brucei with
Mice(28-35g) PBS (ph 7.4) for 30days
(60-65 mice sacrificed)
treated with
Dose of diaminazine aceturate (Berenil) (10mg kg)
5
6. Left half of the mouse brain
5% Buffered formalin
Fore brain hind brain
mid brain
Hematoxylin & Eosin
Stained with
Rehydrated in
3% H202 for 5mins
Rinsed with
PBS
6
7. PBS (PH- 7.4)
incubated with
20% Swine serum (30mins)
DAKO:PBS(1:1000) (Dilution)
1% Bovine serum albumin
placed & left overnight at 4℃.
7
8. right half of the brain
2ml denaturing solution( 4m guadinum
thiocyanate,25mm sodium citrate,0.5% sarcosyl,
0.1m 2-mercapto ethanol) & homogenized.
homogenized
200 μliter of 2m sodium acetate + 2ml water saturate
phenol + 400 μliter of chloroform.
Mixture left on ice for 15 mins
Centrifugation at 1000rpm for 20mins at 4℃
Ice cold isopropanol added
RNA precipitated at -70℃ for 30mins
8
9. RNA pellet suspended in 300microliter of sterile water &
extracted with phenol chloroform
Aqueous layer precipitated with 30 μliter of 7m
ammonium acetate & 600μl absolute ethanol at -70℃
Washed twice in 70% ethanol, put in
200μliter sterile water.100μg of total
RNA would yield.
9
10. By using PCR, we detected a range of cytokine RNA transcripts.
Transcripts for β-actin were detected in the brains of all the infected
& uninfected controls.
IL-1α transcripts were detected in 6 of the 10 uninfected controls,
but no transcripts for TNF- α, IFN- γ, MIP-1, IL-2, IL-4, IL-6 were
detected.
Analysis of RNA samples from the 10 infected mice which had
developed chronic meningo encephalitis showed the presence of
RNA trascripts for IL-1 α,IL-4, TNF- α, MIP-1 in all of these mice.
10
11. IL-6 was found in only samples 4 & 8. while IFN-γ was detected
strongly in only one sample.
Although sample 9 displayed a faint band of appropriate size IL-2
mRNA was not detected in any of these samples.
There are several possible sources of various cytokines, activated
astrocytes in the brain of infected animals, large no. of monocytes
which are capable of synthesizing IL-1α & TNF- α. Presence of these
cytokines can initiate the inflammatory process.
CONCLUSION :
However, in view of the high level of astrocytes activation observed,
it seems likely that astrocytes contribute in some way to the
presence of cytokines & play a role in initiating the inflammatory
processes.
11
12. Detection of IL-1(625bp)(A), IL-4
(399bp)(B), TNF(692bp)(C), MIP-
1(267bp)(D) in the brains of T.b.
brucei effcted mice with meningo-
encephalitis. The left most lanes
(M) contained a ladder of 123bp
fragments. A negative control &
positive control were also included.
12