Properties of cm, plateau potential & pacemaker by Pandian M this PPT for I ...Pandian M
Describe the properties of cardiac muscle including its morphology, electrical, mechanical and metabolic functions SLOs: After attending lecture & studying the assigned materials, the student will: 1.Describe the general features of cardiac muscle. 2.Discuss the light and electron microscopic appearance of cardiac muscle, characteristic features of sarcotubular system. 3.Enlist the electrical properties of heart muscle. 4.Explain the phases of cardiac muscle action potential 5.Explain the nodal action potential. 6.Differentiate between cardiac muscle A.P. and nodal A.P., effect of nervous innervation and ions on AP. 7.Enumerate and explain the mechanical properties of heart muscle, metabolic functions, characteristic features.
Action potential By Dr. Mrs. Padmaja R Desai Physiology Dept
To study the Concept of Action Potential and describe the stages of action potential.
Ionic basis of Action Potential & its Propogation.
Properties of Action Potential.
Types action Potential
Action potential (the guyton and hall physiology)Maryam Fida
ACTION POTENTIAL
Action potential is abrupt pulse like change in the membrane potential lasting for a fraction of second
During action potential there is reversal of membrane potential i.e. inside becomes positive and outside becomes Negative.
We can see the action potential on cathode ray oscilloscope
Abrupt or sudden in onset
2. Have limited magnitude or amplitude i.e. Inside, the potential will go to + 35 or + 45 mV and not beyond that.
3. It is of short duration. Duration is in milli seconds. Duration of spike potential Is 1 -2 milli second. Action potential with plateau has longer duration i.e. may be up to 300 m sec
4. It obeys All or None law i.e. if stimulus is sub threshold it is not produced and when the stimulus is threshold or supra threshold it will be produced with maximum amplitude.
5. It is self propagated i.e. once produced in a membrane it is automatically propagated in both directions.
6. It is not decremented with distance i.e. it will travel with same amplitude through all the distance.
7. It has refractory period. The period during which the tissue will not respond to second stimulus after the application of first stimulus. It could be Absolute and Refractory.
Absolute no response of tissue what so ever may be the strength of stimulus example closure of inactivation gate of sodium channels.
Relative response with higher stimulus than threshold stimulus
DEPOLARIZATION: Sudden loss of Negativity inside the membrane is depolarization.
REPOLARIZATION: return of negativity inside the membrane is Repolarization.
HYPERPOLARIZATION: More Negativity inside
Resting Membrane Potential
Understanding of
Channels Involved
Voltage gated Sodium Channels
Voltage gated Potassium Channels
Sodium Potassium ATPase Pump
Movements of ions
Concentrations of Sodium and Potassium in ECF and ICF
Direction of movement
Plateau is known as Sustained depolarization.
In some instances, the excited membrane does not repolarize immediately after depolarization.
Duration of depolarization of cardiac muscle is 300 milli sec.
Plateau phase has got advantages:
1. It prolongs the duration of depolarization, AP and Contraction. It prolongs the refractory period. Cardiac muscle cannot be tetanized because of this.
2. There is influx of calcium into the sarcoplasm from the ECF which is used for muscle contraction.
Properties of cm, plateau potential & pacemaker by Pandian M this PPT for I ...Pandian M
Describe the properties of cardiac muscle including its morphology, electrical, mechanical and metabolic functions SLOs: After attending lecture & studying the assigned materials, the student will: 1.Describe the general features of cardiac muscle. 2.Discuss the light and electron microscopic appearance of cardiac muscle, characteristic features of sarcotubular system. 3.Enlist the electrical properties of heart muscle. 4.Explain the phases of cardiac muscle action potential 5.Explain the nodal action potential. 6.Differentiate between cardiac muscle A.P. and nodal A.P., effect of nervous innervation and ions on AP. 7.Enumerate and explain the mechanical properties of heart muscle, metabolic functions, characteristic features.
Action potential By Dr. Mrs. Padmaja R Desai Physiology Dept
To study the Concept of Action Potential and describe the stages of action potential.
Ionic basis of Action Potential & its Propogation.
Properties of Action Potential.
Types action Potential
Action potential (the guyton and hall physiology)Maryam Fida
ACTION POTENTIAL
Action potential is abrupt pulse like change in the membrane potential lasting for a fraction of second
During action potential there is reversal of membrane potential i.e. inside becomes positive and outside becomes Negative.
We can see the action potential on cathode ray oscilloscope
Abrupt or sudden in onset
2. Have limited magnitude or amplitude i.e. Inside, the potential will go to + 35 or + 45 mV and not beyond that.
3. It is of short duration. Duration is in milli seconds. Duration of spike potential Is 1 -2 milli second. Action potential with plateau has longer duration i.e. may be up to 300 m sec
4. It obeys All or None law i.e. if stimulus is sub threshold it is not produced and when the stimulus is threshold or supra threshold it will be produced with maximum amplitude.
5. It is self propagated i.e. once produced in a membrane it is automatically propagated in both directions.
6. It is not decremented with distance i.e. it will travel with same amplitude through all the distance.
7. It has refractory period. The period during which the tissue will not respond to second stimulus after the application of first stimulus. It could be Absolute and Refractory.
Absolute no response of tissue what so ever may be the strength of stimulus example closure of inactivation gate of sodium channels.
Relative response with higher stimulus than threshold stimulus
DEPOLARIZATION: Sudden loss of Negativity inside the membrane is depolarization.
REPOLARIZATION: return of negativity inside the membrane is Repolarization.
HYPERPOLARIZATION: More Negativity inside
Resting Membrane Potential
Understanding of
Channels Involved
Voltage gated Sodium Channels
Voltage gated Potassium Channels
Sodium Potassium ATPase Pump
Movements of ions
Concentrations of Sodium and Potassium in ECF and ICF
Direction of movement
Plateau is known as Sustained depolarization.
In some instances, the excited membrane does not repolarize immediately after depolarization.
Duration of depolarization of cardiac muscle is 300 milli sec.
Plateau phase has got advantages:
1. It prolongs the duration of depolarization, AP and Contraction. It prolongs the refractory period. Cardiac muscle cannot be tetanized because of this.
2. There is influx of calcium into the sarcoplasm from the ECF which is used for muscle contraction.
these slides contain a brief introduction of neurons and its classification as well as details of generation of action potential, resting potential and eletrotonic potential.
Cardiac muscle (The Guyton and Hall Physiology)Maryam Fida
In the heart there is Atrial muscle and Ventricular muscle which are separated from each other by the fibrous AV Rings containing Valves.
ATRIAL MUSCLE: thin walled. There are two sheets, superficial and deep sheet. Superficial sheet is common over both atria. Deep sheet is separate for each atrium. Muscle fibers in the deep sheet are at right angle to the muscle fibers in the superficial sheet.
FUNCTIONS OF THE ATRIUM:
1. Receive venous blood from large veins. So atria act as reservoir.
2. Conduct the blood into the ventricles.
3. Atrial contraction is responsible for last 25 % of ventricular filling.
4. In the right atrium there is SA Node(Pace maker) and AV node.
5. In the wall of the atria, there are low pressure stretch receptors and these are involved in various reflexes like brain bridge reflex and left atrial reflex.
6. Atria also produce a hormone i.e. Atrial Natriuretic Hormone. Whenever NaCl increases in ECF, it causes release of ANH which causes natriuresis.
VENTRICULAR MUSCLE:
Much thicker than atrial muscle. Thickness of right ventricle wall is 3-4 mm and thickness of left ventricle is 8 – 12 mm.
1.Involuntary
2.Has cross striations
3.Each cardiac muscle fiber consists of a number of cardiac cells, united at ends in series. Where as in skeletal muscle each muscle fiber is individual cell.
4.Cardiac muscle cells are branching and interdigitate.
5.Single central nucleus in each cell.
6. Atrial muscle and ventricular muscle act as separate functional syncytium and impulses from atria are conducted to ventricles through the AV Node and AV Bundle.
7. Sarcoplasmic system is present. In skeletal muscle triad is at the junction of A and I bands. In cardiac muscle T Tubules are much large and thus in cardiac muscle if we take a section it may form a diad or a triad. And these diads and triads are present at the level of Z Disks.
8.Between adjacent cardiac cells there are side to side and end to end connections and these are the intercellular junctions. These junctions are Gap Junctions. Or intercalated discs
9.When one part of myocardium is excited the whole muscle is excited.
10.Whole myocardium obeys all or none law as a whole.
11.No spike potential but action potential with plateau.
12.Has got long refractory period.
Absolute refractory period in ventricular muscle is 250 – 300 milli sec.
In atrial muscle Absolute refractory period is 150 milli sec
Because of long refractory period cardiac muscle cannot be tetanized.
It is over 60 years since Hodgkin and
Huxley1 made the first direct recording of
the electrical changes across the neuronal
membrane that mediate the action
potential. Using an electrode placed inside a
squid giant axon they were able to measure a
transmembrane potential of around 260 mV
inside relative to outside, under resting
conditions (this is called the resting membrane
potential). The action potential is a
transient (,1 millisecond) reversal in the
polarity of this transmembrane potential
which then moves from its point of initiation,
down the axon, to the axon terminals. In a
subsequent series of elegant experiments
Hodgkin and Huxley, along with Bernard
Katz, discovered that the action potential
results from transient changes in the permeability
of the axon membrane to sodium (Na+)
and potassium (K+) ions. Importantly, Na+ and
K+ cross the membrane through independent
pathways that open in response to a change
in membrane potential.
As testimony to their pioneering work, the
fundamental mechanisms described by
Hodgkin, Huxley and Katz remain applicable
to all excitable cells today. Indeed, the
predictions they made about the molecular
mechanisms that might underlie the changes
in membrane permeability showed remarkable
foresight. The molecular basis of the action
potential lies in the presence of proteins
called ion channels that form the permeation
pathways across the neuronal membrane.
Although the first electrophysiological
recordings from individual ion channels were
not made until the mid 1970s,2 Hodgkin and
Huxley predicted many of the properties now
known to be key components of their
function: ion selectivity, the electrical basis
of voltage-sensitivity and, importantly, a
mechanism for quickly closing down the
permeability pathways to ensure that the
action potential only moves along the axon in
one direction.
Classification of nerve fibers, Nervous System PhysiologyShaista Jabeen
https://www.youtube.com/channel/UCrrAABI7QDRCJ1yMrQCip_w/videos
https://www.facebook.com/ShaistaJabeeen/
https://www.facebook.com/Human-Physiology-Lectures-100702741804409/
Classification of nerve fibers
Nervous System Physiology
BASIS OF CLASSIFICATION
DEPENDING UPON STRUCTURE
DEPENDING UPON DISTRIBUTION
DEPENDING UPON ORIGIN
DEPENDING UPON FUNCTION
DEPENDING UPON SECRETION OF NEUROTRANSMITTER
DEPENDING UPON DIAMETER AND CONDUCTION OF IMPULSE
Short Notes
pdf ppt
1.Describe and then compare and contrast the action potentials of th.pdffathimaoptical
1.Describe and then compare and contrast the action potentials of the primary cardiac pacemaker
and primary contractile cells of the heart.
Solution
Cells within the sinoatrial (SA) node are the primary pacemaker site within the heart. These cells
are characterized as having no true resting potential, but instead generate regular, spontaneous
action potentials. Unlike non-pacemaker action potentials in the heart, and most other cells that
elicit action potentials (e.g., nerve cells, muscle cells), the depolarizing current is carried into the
cell primarily by relatively slow Ca++ currents instead of by fast Na+ currents. There are, in fact,
no fast Na+ channels and currents operating in SA nodal cells. This results in slower action
potentials in terms of how rapidly they depolarize. Therefore, these pacemaker action potentials
are sometimes referred to as \"slow response\" action potentials.
SA nodal action potentials are divided into three phases. Phase 4 is the spontaneous
depolarization (pacemaker potential) that triggers the action potential once the membrane
potential reaches threshold between -40 and -30 mV). Phase 0 is the depolarization phase of the
action potential. This is followed by phase 3 repolarization. Once the cell is completely
repolarized at about -60 mV, the cycle is spontaneously repeated.
The changes in membrane potential during the different phases are brought about by changes in
the movement of ions (principally Ca++ and K+, and to a lesser extent Na+) across the
membrane through ion channels that open and close at different times during the action potential.
When a channel is opened, there is increased electrical conductance (g) of specific ions through
that ion channel. Closure of ion channels causes ion conductance to decrease. As ions flow
through open channels, they generate electrical currents (i or I) that change the membrane
potential.
In the SA node, three ions are particularly important in generating the pacemaker action
potential. They have role of these ions in the different action potential phases.
At the end of repolarization, when the membrane potential is very negative (about -60 mV), ion
channels open that conduct slow, inward (depolarizing) Na+ currents. These currents are called
\"funny\" currents and abbreviated as \"If\". These depolarizing currents cause the membrane
potential to begin to spontaneously depolarize, thereby initiating Phase 4. As the membrane
potential reaches about -50 mV, another type of channel opens. This channel is called transient
or T-type Ca++ channel. As Ca++ enters the cell through these channels down its
electrochemical gradient, the inward directed Ca++ currents further depolarize the cell. When the
membrane depolarizes to about -40 mV, a second type of Ca++ channel opens. These are the so-
called long-lasting, or L-type Ca++ channels. Opening of these channels causes more Ca++ to
enter the cell and to further depolarize the cell until an action potential threshold is re.
these slides contain a brief introduction of neurons and its classification as well as details of generation of action potential, resting potential and eletrotonic potential.
Cardiac muscle (The Guyton and Hall Physiology)Maryam Fida
In the heart there is Atrial muscle and Ventricular muscle which are separated from each other by the fibrous AV Rings containing Valves.
ATRIAL MUSCLE: thin walled. There are two sheets, superficial and deep sheet. Superficial sheet is common over both atria. Deep sheet is separate for each atrium. Muscle fibers in the deep sheet are at right angle to the muscle fibers in the superficial sheet.
FUNCTIONS OF THE ATRIUM:
1. Receive venous blood from large veins. So atria act as reservoir.
2. Conduct the blood into the ventricles.
3. Atrial contraction is responsible for last 25 % of ventricular filling.
4. In the right atrium there is SA Node(Pace maker) and AV node.
5. In the wall of the atria, there are low pressure stretch receptors and these are involved in various reflexes like brain bridge reflex and left atrial reflex.
6. Atria also produce a hormone i.e. Atrial Natriuretic Hormone. Whenever NaCl increases in ECF, it causes release of ANH which causes natriuresis.
VENTRICULAR MUSCLE:
Much thicker than atrial muscle. Thickness of right ventricle wall is 3-4 mm and thickness of left ventricle is 8 – 12 mm.
1.Involuntary
2.Has cross striations
3.Each cardiac muscle fiber consists of a number of cardiac cells, united at ends in series. Where as in skeletal muscle each muscle fiber is individual cell.
4.Cardiac muscle cells are branching and interdigitate.
5.Single central nucleus in each cell.
6. Atrial muscle and ventricular muscle act as separate functional syncytium and impulses from atria are conducted to ventricles through the AV Node and AV Bundle.
7. Sarcoplasmic system is present. In skeletal muscle triad is at the junction of A and I bands. In cardiac muscle T Tubules are much large and thus in cardiac muscle if we take a section it may form a diad or a triad. And these diads and triads are present at the level of Z Disks.
8.Between adjacent cardiac cells there are side to side and end to end connections and these are the intercellular junctions. These junctions are Gap Junctions. Or intercalated discs
9.When one part of myocardium is excited the whole muscle is excited.
10.Whole myocardium obeys all or none law as a whole.
11.No spike potential but action potential with plateau.
12.Has got long refractory period.
Absolute refractory period in ventricular muscle is 250 – 300 milli sec.
In atrial muscle Absolute refractory period is 150 milli sec
Because of long refractory period cardiac muscle cannot be tetanized.
It is over 60 years since Hodgkin and
Huxley1 made the first direct recording of
the electrical changes across the neuronal
membrane that mediate the action
potential. Using an electrode placed inside a
squid giant axon they were able to measure a
transmembrane potential of around 260 mV
inside relative to outside, under resting
conditions (this is called the resting membrane
potential). The action potential is a
transient (,1 millisecond) reversal in the
polarity of this transmembrane potential
which then moves from its point of initiation,
down the axon, to the axon terminals. In a
subsequent series of elegant experiments
Hodgkin and Huxley, along with Bernard
Katz, discovered that the action potential
results from transient changes in the permeability
of the axon membrane to sodium (Na+)
and potassium (K+) ions. Importantly, Na+ and
K+ cross the membrane through independent
pathways that open in response to a change
in membrane potential.
As testimony to their pioneering work, the
fundamental mechanisms described by
Hodgkin, Huxley and Katz remain applicable
to all excitable cells today. Indeed, the
predictions they made about the molecular
mechanisms that might underlie the changes
in membrane permeability showed remarkable
foresight. The molecular basis of the action
potential lies in the presence of proteins
called ion channels that form the permeation
pathways across the neuronal membrane.
Although the first electrophysiological
recordings from individual ion channels were
not made until the mid 1970s,2 Hodgkin and
Huxley predicted many of the properties now
known to be key components of their
function: ion selectivity, the electrical basis
of voltage-sensitivity and, importantly, a
mechanism for quickly closing down the
permeability pathways to ensure that the
action potential only moves along the axon in
one direction.
Classification of nerve fibers, Nervous System PhysiologyShaista Jabeen
https://www.youtube.com/channel/UCrrAABI7QDRCJ1yMrQCip_w/videos
https://www.facebook.com/ShaistaJabeeen/
https://www.facebook.com/Human-Physiology-Lectures-100702741804409/
Classification of nerve fibers
Nervous System Physiology
BASIS OF CLASSIFICATION
DEPENDING UPON STRUCTURE
DEPENDING UPON DISTRIBUTION
DEPENDING UPON ORIGIN
DEPENDING UPON FUNCTION
DEPENDING UPON SECRETION OF NEUROTRANSMITTER
DEPENDING UPON DIAMETER AND CONDUCTION OF IMPULSE
Short Notes
pdf ppt
1.Describe and then compare and contrast the action potentials of th.pdffathimaoptical
1.Describe and then compare and contrast the action potentials of the primary cardiac pacemaker
and primary contractile cells of the heart.
Solution
Cells within the sinoatrial (SA) node are the primary pacemaker site within the heart. These cells
are characterized as having no true resting potential, but instead generate regular, spontaneous
action potentials. Unlike non-pacemaker action potentials in the heart, and most other cells that
elicit action potentials (e.g., nerve cells, muscle cells), the depolarizing current is carried into the
cell primarily by relatively slow Ca++ currents instead of by fast Na+ currents. There are, in fact,
no fast Na+ channels and currents operating in SA nodal cells. This results in slower action
potentials in terms of how rapidly they depolarize. Therefore, these pacemaker action potentials
are sometimes referred to as \"slow response\" action potentials.
SA nodal action potentials are divided into three phases. Phase 4 is the spontaneous
depolarization (pacemaker potential) that triggers the action potential once the membrane
potential reaches threshold between -40 and -30 mV). Phase 0 is the depolarization phase of the
action potential. This is followed by phase 3 repolarization. Once the cell is completely
repolarized at about -60 mV, the cycle is spontaneously repeated.
The changes in membrane potential during the different phases are brought about by changes in
the movement of ions (principally Ca++ and K+, and to a lesser extent Na+) across the
membrane through ion channels that open and close at different times during the action potential.
When a channel is opened, there is increased electrical conductance (g) of specific ions through
that ion channel. Closure of ion channels causes ion conductance to decrease. As ions flow
through open channels, they generate electrical currents (i or I) that change the membrane
potential.
In the SA node, three ions are particularly important in generating the pacemaker action
potential. They have role of these ions in the different action potential phases.
At the end of repolarization, when the membrane potential is very negative (about -60 mV), ion
channels open that conduct slow, inward (depolarizing) Na+ currents. These currents are called
\"funny\" currents and abbreviated as \"If\". These depolarizing currents cause the membrane
potential to begin to spontaneously depolarize, thereby initiating Phase 4. As the membrane
potential reaches about -50 mV, another type of channel opens. This channel is called transient
or T-type Ca++ channel. As Ca++ enters the cell through these channels down its
electrochemical gradient, the inward directed Ca++ currents further depolarize the cell. When the
membrane depolarizes to about -40 mV, a second type of Ca++ channel opens. These are the so-
called long-lasting, or L-type Ca++ channels. Opening of these channels causes more Ca++ to
enter the cell and to further depolarize the cell until an action potential threshold is re.
Presentation on cardiac system of human bodyitromalinda
Cross Bridge Cycle
In presence of calcium, myosin head binds to an actin filament
Changes its orientation relative to myosin filament which causes filaments to slide relative to each other - Power Stroke
During the Cross-Bridge Cycle, Contractile Proteins Convert the Energy of ATP Hydrolysis into Mechanical Energy
Each power stroke shortens sarcomere by 10nm
Cross bridge cycling is asynchronous
• 500 myosin in one thick filament, each head cycling 5 times per second
The action potential inhibits the calcium pumps, and calcium escapes from the sareophismic reticulum.
Cross Bridge Cycle
Occurs in 5 steps:-
1. Cross - Bridge formation
• cocked myosin head (perpendicular or at a 90-degree angle to the thick and thin filaments) binds to actin filament
Cocked head has the stored energy derived from the cleaved ATP
Cross Bridge Cycle
Release of Pi from the myosin
2. Dissociation of Pi from the myosin head triggers power stroke
Conformational change - myosin head bends approximately 450 about the hinge
Pulls the actin filament about 11 nm toward the tail of the myosin molecule
Generating force and motion.
Cross Bridge Cycle
ADP release –
Dissociation of ADP from myosin
Myosin head remains in the same position (45° angle with respect to the thick and thin filaments)
3. ATP binding –
ATP binding to the head of the myosin heavy chain (MHC) reduces the affinity of myosin for actin
Myosin head releases actin filament
Cross Bridge Cycle
ATP hydrolysis
Breakdown of ATP to ADP and inorganic phosphate (Pi) occurs on myosin head
Products of hydrolysis are retained on the myosin
As a result of hydrolysis, the myosin head pivots around the hinge into a "cocked" position (perpendicular or at a 900 angle to the thick and thin filaments)
Rotation causes the tip of the myosin to move about 11 nm along the actin filament so that it now lines up with a new actin monomer two monomers further along the actin filament
Cross Bridge Cycle
Cycle repeats as long as Ca, is elevated and sufficient ATP is there
Muscle cells do not regulate cross-bridge cycling by modifying [ATP]i
Instead, skeletal muscle and cardiac muscle control this cycle by preventing cross-bridge formation until the tropomyosin moves out of the way in response to an increase in [Ca']i
Steps in Relaxation
Cell may extrude Ca,- using either an Na-Ca exchanger (NCX) or a Ca' pump(PMCA)
However, would eventually deplete the cell of Ca, and is thus a minor mechanism for Ca, removal from the cytoplasm
Instead, Ca, re-uptake into the SR is the most important mechanism by which the cell returns [Ca']i to resting levels
Ca' re-uptake by the SR is mediated by a SERCA(s arcoplasmic or e ndoplasmic r eticulum C a2+8 TPase )-type Ca' pump
Steps in Relaxation
SR Ca2+-pump activity is inhibited by high [Ca2*] within the SR lumen
Inhibition of SR
Ca2+-pump activity is delayed by
Ca?+-binding proteins within the SR lumen = Buffer the Ca?* increase in the SR during Ca
A summary of skeletal muscle contraction and relaxationAyub Abdi
it consist for 4 pages and cover all the steps that occur during muscle contraction and relaxation, I does not take a time just 5 minute is enough to read. I hope it's interesting.
Muscle contraction is very important to do our daily activity every should understand how and what factors contribute for developing muscle contraction and relaxation.
in this presentation you will learns the neuromuscular junction and how excitation contraction coupling occurs.
The body's balance between acidity and alkalinity is referred to as acid-base balance. The blood's acid-base balance is precisely controlled because even a minor deviation from the normal range can severely affect many organs. The body uses different mechanisms to control the blood's acid-base balance.
Muscle spindles are proprioceptors that consist of intrafusal muscle fibers enclosed in a sheath (spindle). They run parallel to the extrafusal muscle fibers and act as receptors that provide information on muscle length and the rate of change in muscle length. The spindles are stretched when the muscle lengthens. This stretch causes the sensory neuron in the spindle to transmit an impulse to the spinal cord, where it synapses with alpha motor neurons. This causes activation of motor neurons that innervate the muscle. The muscle spindles determine the amount of contraction necessary to overcome a given resistance. When the resistance increases, the muscle is stretched further, and this causes spindle fibers to activate a greater muscle contraction.
Have you ever wondered why you sweat when you get too hot from running or shiver on a cold winter's day in this video we are going to explain why your body behaves like this.
Humans are endotherms and this means we are warm blooded we keep our body operating at thirty seven degrees Celsius regardless of the external conditions however this is a real challenge as our environment changes all the time depending on the weather, our clothes, if we are inside by the fire or outside having a snowball fight. So how does this work?
It's quite similar to the heating system in a house. in a house is a thermostat that measures the temperature if the house gets cold the thermostat will tell the radiators to turn on and heat it up if it's too hot they will be told to switch off simple.
Your body works in just the same way here in your brain as a special area called the hypothalamus and it measures the temperature of the blood flowing through it and also it collects information from temperatures senses around the body. it then decides if the temperature is too hot or too cold and we'll try and bring it back to thirty seven degrees Celsius. If you are too hot the hypothalamus can then send signals out to the body by the nervous system that can cause barriers to fact. It can send a signal to your skin and cool sweat glands to secrete the sweat on to the surface of the skin the sweat itself is not cold but it works because it takes the heat away from your body in order to evaporate it.
Another way of losing is vasodilation let kind of these blood vessels narrows this. That said the skin open white and allow blood to flow through them. They heat is radiated from the blood into the air and the blood cools down. If you get too cold you can do the opposite with these blood vessels and place them on keeping the blood away from the surface of the skin this is called vasoconstriction this is when your muscles contract in order to make. Another fact you may have noticed when you are cold against them. If you look more place the at least the Bulls what you realized is that each of the little bugger has a has to hit out at.
These has stood up on and struck a layer of air around the skin air is a fantastic insulate of heat and this will keep you nice and warm.
A brief information about the SCOP protein database used in bioinformatics.
The Structural Classification of Proteins (SCOP) database is a comprehensive and authoritative resource for the structural and evolutionary relationships of proteins. It provides a detailed and curated classification of protein structures, grouping them into families, superfamilies, and folds based on their structural and sequence similarities.
Seminar of U.V. Spectroscopy by SAMIR PANDASAMIR PANDA
Spectroscopy is a branch of science dealing the study of interaction of electromagnetic radiation with matter.
Ultraviolet-visible spectroscopy refers to absorption spectroscopy or reflect spectroscopy in the UV-VIS spectral region.
Ultraviolet-visible spectroscopy is an analytical method that can measure the amount of light received by the analyte.
(May 29th, 2024) Advancements in Intravital Microscopy- Insights for Preclini...Scintica Instrumentation
Intravital microscopy (IVM) is a powerful tool utilized to study cellular behavior over time and space in vivo. Much of our understanding of cell biology has been accomplished using various in vitro and ex vivo methods; however, these studies do not necessarily reflect the natural dynamics of biological processes. Unlike traditional cell culture or fixed tissue imaging, IVM allows for the ultra-fast high-resolution imaging of cellular processes over time and space and were studied in its natural environment. Real-time visualization of biological processes in the context of an intact organism helps maintain physiological relevance and provide insights into the progression of disease, response to treatments or developmental processes.
In this webinar we give an overview of advanced applications of the IVM system in preclinical research. IVIM technology is a provider of all-in-one intravital microscopy systems and solutions optimized for in vivo imaging of live animal models at sub-micron resolution. The system’s unique features and user-friendly software enables researchers to probe fast dynamic biological processes such as immune cell tracking, cell-cell interaction as well as vascularization and tumor metastasis with exceptional detail. This webinar will also give an overview of IVM being utilized in drug development, offering a view into the intricate interaction between drugs/nanoparticles and tissues in vivo and allows for the evaluation of therapeutic intervention in a variety of tissues and organs. This interdisciplinary collaboration continues to drive the advancements of novel therapeutic strategies.
THE IMPORTANCE OF MARTIAN ATMOSPHERE SAMPLE RETURN.Sérgio Sacani
The return of a sample of near-surface atmosphere from Mars would facilitate answers to several first-order science questions surrounding the formation and evolution of the planet. One of the important aspects of terrestrial planet formation in general is the role that primary atmospheres played in influencing the chemistry and structure of the planets and their antecedents. Studies of the martian atmosphere can be used to investigate the role of a primary atmosphere in its history. Atmosphere samples would also inform our understanding of the near-surface chemistry of the planet, and ultimately the prospects for life. High-precision isotopic analyses of constituent gases are needed to address these questions, requiring that the analyses are made on returned samples rather than in situ.
The increased availability of biomedical data, particularly in the public domain, offers the opportunity to better understand human health and to develop effective therapeutics for a wide range of unmet medical needs. However, data scientists remain stymied by the fact that data remain hard to find and to productively reuse because data and their metadata i) are wholly inaccessible, ii) are in non-standard or incompatible representations, iii) do not conform to community standards, and iv) have unclear or highly restricted terms and conditions that preclude legitimate reuse. These limitations require a rethink on data can be made machine and AI-ready - the key motivation behind the FAIR Guiding Principles. Concurrently, while recent efforts have explored the use of deep learning to fuse disparate data into predictive models for a wide range of biomedical applications, these models often fail even when the correct answer is already known, and fail to explain individual predictions in terms that data scientists can appreciate. These limitations suggest that new methods to produce practical artificial intelligence are still needed.
In this talk, I will discuss our work in (1) building an integrative knowledge infrastructure to prepare FAIR and "AI-ready" data and services along with (2) neurosymbolic AI methods to improve the quality of predictions and to generate plausible explanations. Attention is given to standards, platforms, and methods to wrangle knowledge into simple, but effective semantic and latent representations, and to make these available into standards-compliant and discoverable interfaces that can be used in model building, validation, and explanation. Our work, and those of others in the field, creates a baseline for building trustworthy and easy to deploy AI models in biomedicine.
Bio
Dr. Michel Dumontier is the Distinguished Professor of Data Science at Maastricht University, founder and executive director of the Institute of Data Science, and co-founder of the FAIR (Findable, Accessible, Interoperable and Reusable) data principles. His research explores socio-technological approaches for responsible discovery science, which includes collaborative multi-modal knowledge graphs, privacy-preserving distributed data mining, and AI methods for drug discovery and personalized medicine. His work is supported through the Dutch National Research Agenda, the Netherlands Organisation for Scientific Research, Horizon Europe, the European Open Science Cloud, the US National Institutes of Health, and a Marie-Curie Innovative Training Network. He is the editor-in-chief for the journal Data Science and is internationally recognized for his contributions in bioinformatics, biomedical informatics, and semantic technologies including ontologies and linked data.
Nutraceutical market, scope and growth: Herbal drug technologyLokesh Patil
As consumer awareness of health and wellness rises, the nutraceutical market—which includes goods like functional meals, drinks, and dietary supplements that provide health advantages beyond basic nutrition—is growing significantly. As healthcare expenses rise, the population ages, and people want natural and preventative health solutions more and more, this industry is increasing quickly. Further driving market expansion are product formulation innovations and the use of cutting-edge technology for customized nutrition. With its worldwide reach, the nutraceutical industry is expected to keep growing and provide significant chances for research and investment in a number of categories, including vitamins, minerals, probiotics, and herbal supplements.
Cancer cell metabolism: special Reference to Lactate PathwayAADYARAJPANDEY1
Normal Cell Metabolism:
Cellular respiration describes the series of steps that cells use to break down sugar and other chemicals to get the energy we need to function.
Energy is stored in the bonds of glucose and when glucose is broken down, much of that energy is released.
Cell utilize energy in the form of ATP.
The first step of respiration is called glycolysis. In a series of steps, glycolysis breaks glucose into two smaller molecules - a chemical called pyruvate. A small amount of ATP is formed during this process.
Most healthy cells continue the breakdown in a second process, called the Kreb's cycle. The Kreb's cycle allows cells to “burn” the pyruvates made in glycolysis to get more ATP.
The last step in the breakdown of glucose is called oxidative phosphorylation (Ox-Phos).
It takes place in specialized cell structures called mitochondria. This process produces a large amount of ATP. Importantly, cells need oxygen to complete oxidative phosphorylation.
If a cell completes only glycolysis, only 2 molecules of ATP are made per glucose. However, if the cell completes the entire respiration process (glycolysis - Kreb's - oxidative phosphorylation), about 36 molecules of ATP are created, giving it much more energy to use.
IN CANCER CELL:
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
introduction to WARBERG PHENOMENA:
WARBURG EFFECT Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside.
Otto Heinrich Warburg (; 8 October 1883 – 1 August 1970) In 1931 was awarded the Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme.
WARNBURG EFFECT : cancer cells under aerobic (well-oxygenated) conditions to metabolize glucose to lactate (aerobic glycolysis) is known as the Warburg effect. Warburg made the observation that tumor slices consume glucose and secrete lactate at a higher rate than normal tissues.
This pdf is about the Schizophrenia.
For more details visit on YouTube; @SELF-EXPLANATORY;
https://www.youtube.com/channel/UCAiarMZDNhe1A3Rnpr_WkzA/videos
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2. Cardiac Muscle Contraction
▪The action potential initiated by
the SA node travels along the
conduction system and spreads out
to excite the “working” atrial and
ventricular muscle fibers, called
contractile fibers.
3. Depolarization
▪ contractile fibers have a stable resting membrane potential
that is close to -90 mV.
▪ When a contractile fiber is brought to threshold by an
action potential from neighboring fibers, its voltage-gated
Na channels open.
▪ Opening of these channels allows Na+ inflow.
▪ Inflow of Na+ down the electrochemical gradient produces a
rapid depolarization .
▪ Within a few milliseconds, the fast Na+ channels
automatically inactivate and Na+ inflow decreases.
4. Plateau
▪ A period of maintained depolarization.
▪ It is due in part to opening of voltage-gated slow Ca2
channels in the sarcolemma. When these channels open,
calcium ions move from the interstitial fluid into the cytosol.
This inflow of Ca2+ causes even more Ca2+ to pour out of the
sarcoplasmic reticulum into the cytosol through additional
Ca2+ channels in the sarcoplasmic reticulum membrane.
▪ The increased Ca2+ concentration in the cytosol ultimately
triggers contraction.
5. Plateau
▪ Several different types of voltage-gated K channels are also
found in the sarcolemma of a contractile fiber.
▪ Just before the plateau phase begins, some of these K
channels open, allowing potassium ions to leave the
contractile fiber.
▪ Therefore, depolarization is sustained during the plateau
phase because Ca2+ inflow just balances K+ outflow.
▪ By comparison, depolarization in a neuron or skeletal muscle
fiber is much briefer, about 1 msec (0.001 sec), because it
lacks a plateau phase.
6. Repolarization
▪ The recovery of the resting membrane potential during the
repolarization phase of a cardiac action potential resembles
that in other excitable cells. After a delay (which is
particularly prolonged in cardiac muscle), additional voltage-
gated K+ channels open.
▪ Outflow of K+ restores the negative resting membrane
potential (-90 mV).
▪ At the same time, the calcium channels in the sarcolemma
and the sarcoplasmic reticulum are closing, which also
contributes to repolarization.
