The name is derived from Greek word,
Trypano means (borer)
Soma means (body)
They are unicellular flagellate protozoa.
Have corkscrew like motion.
Oftenly transmitted by a vector.
Medical Parasitology
Life cycle, Medical menifestation, signs, Diagnosis and Prevention.
Trypanosoma brucei brucei
Chagas disease
visceral leishmaniasis
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The name is derived from Greek word,
Trypano means (borer)
Soma means (body)
They are unicellular flagellate protozoa.
Have corkscrew like motion.
Oftenly transmitted by a vector.
Medical Parasitology
Life cycle, Medical menifestation, signs, Diagnosis and Prevention.
Trypanosoma brucei brucei
Chagas disease
visceral leishmaniasis
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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.
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
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Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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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.
3. Classification:
• Eukaryota (organisms with
nucleated cells),Kingdom
Protista, Phylum Protozoa.
• East African
trypanosomiasis is caused
by the parasite
Trypanosoma brucei
rhodesiense.
• West African
trypanosomiasis is caused
by Trypanosoma brucei
gambiense. The parasites
are spread by tsetse flies,
found only in Africa.
4. Morphology
Trypanosomes have a single central
nucleusand a single flagellum
originating at the kinetoplast and joined
to the body by an undulatingmembrane.
The outersurface of the organism is
densely coated with a layer of
glycoprotein, the variable surface
glycoprotein (VSG).
From the point of view of functional
and physiologic complexity, a
protozoanis more like an animal than
like a single cell.
5. Morphological Forms
TRYPOMASTIGOTE
• The kinetoplast (kt) is located on the
posteriorend of the parasite. The
flagellum emerges from the posterior
end and folds back along the parasite's
body. This attachment of the flagellum
to the body forms an undulating
membrane (um) that spans the entire
length of the parasite and the free
flagellum emerges from the anterior
end. This is considered the anterior
end since the flagellum pullsthe
organism and the end with the free
flagellum is the front in reference to
the direction of movement. The
undulatingmembrane functions like a
fin and increases the motility of the
organism.
6. Morphological Forms
EPIMASTIGOTE
• The kinetoplast (kt) is more
centrally located, usually just
anterior to nucleus (Nu). The
flagellum (fg) emerges from the
middle of the parasite and forms
a shorter undulating membrane
(um) than observed in
trypomastigotes. Epimastigotes
are noticeably less motile than
trypomastigotes.
7. Morphological Forms
PROMASTIGOTE
• The kinetoplast (kt) is
towards the anterior end and a
free flagellum (fg) with no
undulating membrane
emerges. The end that the free
flagellum emerges from in all
three motile forms is
designated as the anterior end
because they swim in that
direction. In other words, the
flagellum pulls the organism.
8. Morphological Forms
AMASTIGOTE
• The parasite is more spherical in
shape and has no free flagellum.
A basal body (bb) and the base
of the flagellum is still present.
The kinetoplast (kt) is usually
detectable as a darkly staining
body near the nucleus (Nu).
This form is a non-motile
intracellular stage.
9. Etiology.
There are two clinical
forms of African
trypanosomiasis:
• 1) a slowly developing
disease caused by
Trypanosome brucei
gambiense and
• 2) a rapidly progressing
disease caused by T.
brucei rhodesiense.
10. • The Gambian form tends to be more chronic
and sometimes takes several years to develop
central nervous system (CNS) involvement.
11. Major Differences Between African
Trypanosome Species
Attribute T. rhodesiense T. gambiense
tsetse vector G. morsitans group G. palpalis group
ecology dry bush, woodland rainforest, riverine, lakes
transmission cycle ungulate-fly-human human-fly-human
non-human reservoir wild animals domestic animals
epidemiology sporadic, safaris endemic, some epidemics
disease progression rapid, often fatal slow (~1 yr) acute ⇒ chronic
parasitemia high low
asymptomatic carriers rare common
13. Epidemiology
• Human trypanosomiasis has caused massive
epidemics in the past. At the turn of the
century, in Zaire and around Lake Victoria,
large epidemics caused at least three-
quarters of a million deaths. Although only
approximately 20000 cases are reported
each year to the World Health Organization,
gross under-reporting, reduced surveillance,
and recent epidemics in Zaire, Uganda,
Tanzania, Mozambique, and Sudan underline
the continuing importance of human
trypanosomiasis in public health.
Trypanosomiasis of domestic animals and
man remains an important deterrent to
development in endemic areas and shows
increased prevalence associated with war,
civil disturbance, and refugee groups as well
as deteriorating health services and disease-
specific control programmes.
14. EPIDEMIOLOGY
• Genus : Trypanosoma
• Source : sick person
• Transmission:
1. Insect bites: the parasites that cause
sleeping sickness can be transmitted by
the bite of infected tsetse flies
2. Mother-to-child transmission
3. Sexual contact
• Risk group : rural areas
15. • Blood trypomastigotes enter the insect’s body
during the blood-sucking of invaded
vertebrates or humans, which multiply by
binary division in the intestinal lumen of the
tsetse fly.
• By day 3-4, trypomastigotic forms enter the
salivary glands, where they are transformed
into epimastigotes. In the salivary glands,
epimastigous forms undergo multiple divisions
and complex morphologicalchanges, as a
result of which they turn into metacyclic
trypomastigotes, which are an invasive stage
of trypanosomes.
16. PATHOGENESIS
• When bitten again, the tsetse fly, along
with saliva, introduces metacyclic
trypomastigotes under the human skin,
which after a few days enter the blood and
lymph, spread through the body, turning
into blood trypomastigotes.
17. КЛИНИКА
• Incubationperiod – 1 week
• a local inflammatoryreaction develops at the
entrance gate in the form of a painful itchy
chancre (trypanoma, or trypanosomal
chancre), which is a painful erythematous
nodule with a diameter of 1-2 cm,
resembling a boil and regional
lymphadenitis.
• Hemolymphatic stage in 1 – 3 Weeks.
• late (meningoencephalitic)
18. • Trypanids on the trunk and limbs.
• swelling of face and hands.
• Lymphadenitis – posterior cervical
(Winterbottom’s symptom), which become
dense and can reach the size of a pigeon’s egg
19. Clinical Symptoms
• A tsetse fly bite is often painful and
can develop into a red sore, called a
chancre.
• Usually on the head or upper limbs
21. Clinical Symptoms
• Weight loss and a body rash
are also common.
• Infection of the central
nervous system causes
confusion, personality
changes, slurred speech,
seizures, and difficulty in
walking and talking. If left
untreated, the illness
becomes worse, and death
occurs within several weeks
to months
22. Laboratory Diagnostics:
• In the early stages of the disease,
the parasites can be
demonstrated in lymph nodes
and blood; later, they appear in
the cerebrospinal fluid. In the
Rhodesian type, lumbar puncture
is indicated because of early CNS
invasion. Culture or laboratory
animal inoculations can be useful.
Serologic tests, such as indirect
immunofluorescence, direct card
agglutination, and indirect
hemagglutination, are used
successfully for diagnosis.
23.
24. Treatment
• Medicine for the treatment of African trypanosomiasis
is available. Treatment should be started as soon as
possible and is based on the infected person's
symptoms and laboratory tests results.
• Patients need to be hospitalized for treatment and
require periodic follow-up exams for 2 years.
• The current standard treatment for first stage disease
is: Intravenous pentamidine (for T.b. gambiense); or
suramin (for T.b. rhodesiense).
• The current standard treatment for second stage
disease is: Intravenous melarsoprol.
• In areas with melarsoprol resistance or in patients who
have relapsed after melarsoprol monotherapy, the
treatment should be: melarsopsol and nifurtimox, or
eflornithine.
25. Prevention
• There is no vaccine or drug to prevent African
trypanosomiasis.
• When traveling in areas where the disease
occurs, take these precautions against bites
from tsetse flies and other insects.