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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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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
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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2 Case Reports of Gastric Ultrasound
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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3. Definition
• Manifestation of severe plasmodium falciparum malaria
• Unarousable coma more than 30 mts with a glasgow coma scale <7/15
with evidence of acute falciparum infection(asexual form in peripheral
blood smear)
11/25/2010 Cerebral malaria 3
4. Epidemiology
WORLD
300 – 500 million cases ( 90% in Africa)
1.1 - 2.7 million deaths annually
INDIA
2.5 – 3 million cases / yr
1000 deaths / yr ( under estimate )
11/25/2010 Cerebral malaria 4
5. PATHOGENESIS OF
CEREBRAL MALARIA
1. MECHANICAL HYPOTHESIS
Sequestration of RBC in the brain by
cytoadherence / Rosetting
2. Toxin/cytokine HYPOTHESIS
Malarial toxin induced cytokines
stimulating excessive Nitric oxide
Production.
11/25/2010 Cerebral malaria 5
6. MECHANICAL HYPOTHESIS
• Cytoadherence
parasite after invading RBC membrane, 12/15 hrs later protruberances
appear on the erythrocyte’s surface. These “knobs” extrude a high
molecular weight, antigenically variant, strain specific erythrocyte
membrane adhesive protien (pfEMP1) that mediates attachement to
receptors on venular and capillary endothelium. Thus eventually block
capillaries and venules.
• Rosetting
Binding of 2 or more uninfected RBC’s to an infected RBCs.
• Agglutination
The binding of 2/more infected RBC’s.
11/25/2010 Cerebral malaria 6
7. Toxin/cytokine HYPOTHESIS
• Glycolipid material released on merozite rupture initiates cytokine
cascade from macrophages and monocyte series and endothelium with
release of interleukin-1, TNF alpha, interleukin-6 and interleukin-8.
• Evidence of positive correlation cytokine levels and prognosis.
• TNF alpha>100pg/ml is associated with cerebral pathology and death.
11/25/2010 Cerebral malaria 7
8. HUMORAL HYPOTHESIS
MALARIAL TOXIN MACROPHAGE ACTIVATION
TNF alpha & IL – 6
↓
UNCONTROLLED NITRIC OXIDE
PRODUCTION
↓
Nitric Oxide diffuse blood brain barrier
IMPAIRS SYNAPTIC TRANSMISSION
( like general anaesthetics / ethanol )
↓
COMA
11/25/2010 Cerebral malaria 8
9. • CEREBRAL MALARIA MECHANICAL HYPOTHESIS CAN NOT EXPLAIN
RELATIVE ABSENCE OF NEUROLOGICAL DEFICIT EVEN AFTER DAYS OF
COMA.
• TOXIN/CYTOKINE HYPOTHESIS CAN EXPLAIN THE RAPID RECOVERY OF
COMA AND ABSENCE OF NEUROLOGICAL DEFICIT.
11/25/2010 Cerebral malaria 9
10. CLINICAL FEATURES
Onset
Acute – following seizures
Gradual
Consciousness
Drowsiness, confusion, disorientation, delirium and agitation.
Seizures
Repeated genaralised convulsions > 2/24 hrs.
11/25/2010 Cerebral malaria 10
11. OTHER CLINICAL FEATURES
• Mild neck stiffness – no rigidity
• Papilloedema in < 1%
• Retinal hemorrhages – 15 %
• Pupils and corneal reflex – normal
• Transient dysconjugate gaze- no paresis
• Jaw jerk may be brisk
• Forced jaw closure/ Bruxism
• Motor system
- Decorticate rigidity
- Decerebrate rigidity
- opisthotonus
-Tone may be increased, decreased or normal
-Cremasteric and Abdominal reflex normal
-DTR and Plantar reflex variable
11/25/2010 Cerebral malaria 11
12. OTHER CAUSES OF NEUROLOGICAL
DYSFUNCTION
Very high fever – febrile seizures, altered consciousness,Psychosis.
Antimalarial drugs – chloroquine, mefloquine.
HYPOGLYCEMIA – severe parasitemia,quinine.
Hyponatremia – vomiting, elderly patients.
Severe anemia
11/25/2010 Cerebral malaria 12
15. SEQUELE AND POST MALARIAL NEUROLOGICAL
SYNDROMES
3% in adults, 10% in children.
50% recover completely
25% partial recovery
25% no recovery
• Hemiparesis, hemisensory deficits, cotical blindness,
• cranial nerve palsies,(isolated 6th nerve palsy) ,foot drop,
• Extra pyramidal symptoms(chorea,athetosis,tremors)
• Sudden blindeness due to vitreous haemorrhage.
• Cerebellar ataxia
Acute febrile stage - with complete recovery, Delayed onset - 3-4 wks after
malaria
recovers by 3- 16 wks
• Psychiatric disturbances –
Depression, Amnesia, psychosis, personality changes, Delusion and
Hallucinations.
11/25/2010 Cerebral malaria 15
16. Investigaions
Microscopic examination of blood film is gold standard for diagnosis of
malaria.
•Thick blood film
– Species specific and inexpensive.
•Thin blood film
– Rapid, species specific and inexpensive.
•PfHRP2 dipstick card test
– Rapid and sensitive, Detects only p falciparum.
•Role of PCR
– most sensitive and specific
– Results only after 24hrs
11/25/2010 Cerebral malaria 16
17. Microscopy
• Thin blood film • Thick blood film
Schizonts Trophozoite Gamatocytes Schizonts
11/25/2010 Cerebral malaria 17
18. Treatment
• Medical emergency Requires ICU care.
• Ventilatory support, cardiac monitoring.
• Correction of fluids, electrolytes and acid base balance.
• Blood transfusion(where facilities are available)
• Specific treatment
– Artesunate is drug of choice - 2.4mg/kg(2vails) iv at 0hr and 24hrs
then daily till pt can take orally.
– Quinine in case of first trimester of pregnanacy – 20mg/kg in
5%dextrose saline in 4hrs then 8th hrly orally to complete 7 days
– Doxycycline 3.5mg/kg/day for 7 days
– Tetracycline/clindamycin(children and pregnancy)
• ACT- COMBINATION THERAPY
11/25/2010 Cerebral malaria 18
19. CONCLUSION
• Changing profile of clinical features of plasmodium
falciparum – cerebral malaria jaundice / renal failure/
MODS.
• Cytoadherence, rosetting, Nitric oxide and biomass
of brain are important pathogenic mechanisms in cerebral
malaria.
• Quinine & doxy / Artesunate & doxy are effective
combinations in treating cerebral malaria.
11/25/2010 Cerebral malaria 19
