Category Archives: Cell biology and Genetics

Acid-Base Balance Regulation, with Animation

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pH is an indicator of acidity. The body’s blood pH is strictly regulated within a narrow range between 7.35 and 7.45. This is because even a minor change in acidity may have devastating effects on protein stability and biochemical processes.

Normal cellular metabolism constantly produces and excretes carbon dioxide into the blood. Carbon dioxide combines with water to make carbonic acid which dissociates into hydrogen ions and bicarbonate.

CO2 + H2O =  H2CO3 =  H+ + HCO3

This is an equilibrium, meaning all the components of the left and right sides co-exist at all times, and the concentration of any component is determined by that of others at any given moment. The rule of thumb is: an increase in concentration of ANY component on ONE side will shift the equation to the OTHER side, leading to INCREASED concentrations of all components on THAT side, and vice versa. This equilibrium is central to understand acid-base regulation. CONTINUED carbon dioxide production by all cells of the body drives the equilibrium to the right to generate more hydrogen ions. Because pH is basically a function of hydrogen ion concentration, more hydrogen means higher acidity and lower pH. Normal metabolism, therefore, constantly makes the blood more acidic. The body must react to keep the blood pH within the normal limits. This is achieved by 2 mechanisms:

  • Elimination of carbon dioxide through exhalation. The amount of carbon dioxide exhaled by the lungs is regulated in response to changes in acidity. A decrease in pH is sensed by central or arterial chemoreceptors and leads to deeper, faster breathing; more carbon dioxide is exhaled, less hydrogen is made, blood acidity decreases and blood pH returns to normal. Pulmonary regulation is fast, usually effective within minutes to hours.
  • Excretion of hydrogen ions and reabsorption of bicarbonate through the kidneys. The kidneys control blood pH by adjusting the amount of excreted acids and reabsorbed bicarbonate. Renal regulation is slower; it usually takes days to respond to pH disturbances.

Renal regulation: Although all of the plasma bicarbonate is filtered in the glomerulus during the first step of urine formation, virtually ALL of it is REabsorbed BACK into the blood. Most of this reabsorption happens in the proximal tubule. The amount of reabsorbed bicarbonate in the proximal tubule is regulated, via a number of mechanisms, in response to changes in blood pH. It increases during acid loads and decreases during alkali loads. While the proximal tubule basically RETURNS FILTERED bicarbonate back to the blood, the downstream collecting duct generates NEW bicarbonate by ACTIVELY SECRETING acids. As protons are depleted from the distal tubular cells, the equation shifts to the right, producing MORE bicarbonate which then exits into the blood. Hydrogen ions secreted into the lumen combine with urinary buffers, mainly filtered phosphate, and ammonia, to be excreted in urine. The ammonia buffering system is particularly important because unlike phosphate, which is filtered in FIXED amounts from the plasma and can be depleted during high acid loads, ammonia production is regulated in response to changes in acidity and its concentration may increase several folds when necessary. Blood pH is the main regulator of acid excretion, but potassium, chloride concentrations and several hormones also play important roles.

Pathologic changes may cause acid-base disturbances. Acidosis refers to a process that causes increased acidity, while alkalosis refers to one that causes increased alkalinity. It’s not uncommon for a patient to have several processes going on at once, some of them in opposite directions. The resulting plasma pH may be normal; too acidic, called acidemia; or too basic, called alkalemia.

Acidosis may result from INadequate function of the lungs which causes arterial carbon dioxide to accumulate. This is RESPIRATORY acidosis. On the other hand, METABOLIC acidosis may result from excessive production of metabolic acids, DEcreased ability of the kidneys to excrete acids, ingestion of acids, or loss of alkali. Metabolic acidosis is characterized by primary DEcrease in plasma bicarbonate.

Alkalosis can also be either respiratory or metabolic. Respiratory alkalosis is caused by INcreased ventilation resulting in excessive exhalation of carbon dioxide. Metabolic alkalosis can result from excess loss of acids through the kidneys or gastrointestinal tract, bicarbonate retention, or ingestion of alkali. Metabolic alkalosis is characterized by primary increase in plasma bicarbonate.

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Long Term Potentiation and Memory, with Animation

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The process of learning begins with sensory signals being transcribed in the cortex. They are then transmitted to the hippocampus where new memories are believed to form. If a signal is strong, or repeated, a long-term memory is established and wired back to the cortex for storage. Lesions in the hippocampus impair formation of new memories, but do not affect the older ones.
The brain consists of billions of neurons. Neurons communicate with each other through a space between them, called a synapse. A typical neuron can have thousands of synapses, or connections, with other neurons. Together, they form extremely complex networks that are responsible for all brain’s functions. Synaptic connections can change over time, a phenomenon known as synaptic plasticity. Synaptic plasticity follows the “use it or lose it” rule: frequently used synapses are strengthened while rarely used connections are eliminated. Synaptic plasticity is believed to underlie the process of learning and memory retention. New memories are formed when neurons establish new connections, or STRENGTHEN existing synapses. If a memory is no longer needed or rarely recalled, its corresponding synapses will slowly weaken and eventually disappear.
The strength of a synapse is measured by the level of excitability or responsiveness of the post-synaptic neuron in response to a GIVEN stimulus from the pre-synaptic neuron. High-frequency signals or repeated stimulations STRENGTHEN synaptic connections over time. This is known as long-term potentiation, or LTP, and is thought to be the cellular basis of memory formation. LTP can occur at most excitatory synapses all over the brain, but is best studied at the glutamate synapse of the hippocampus.
When a glutamatergic neuron is stimulated, action potentials travel down its axon and trigger the release of glutamate into the synaptic cleft. Glutamate then binds to its receptors on the post-synaptic neuron. The 2 main glutamate receptors that often co-exist in a synapse are AMPA and NMDA receptors. These are ion channels that activate upon binding to glutamate. When the pre-synaptic neuron is stimulated by a WEAK signal, only a small amount of glutamate is released. Although both receptors are bound by the glutamate, only AMPA is activated by weak stimulation. Sodium influx through the AMPA channel results in a SLIGHT DE-polarization of the post-synaptic membrane. The NMDA channel remains closed because its pore is blocked by magnesium ions.
When the pre-synaptic neuron is stimulated by a STRONG or REPEATING signal, a large amount of glutamate is released; the AMPA receptor stays open for a longer time, admitting more sodium into the cell, thus resulting in a GREATER DE-polarization. Increased influx of positive ions EXPELS magnesium from the NMDA channel, which NOW activates, allowing not only sodium but also CALCIUM into the cell. Calcium is the mediator of LTP induction. There are 2 distinct phases of LTP. In the early phase, calcium initiates signaling pathways that activate several protein kinases. These kinases enhance synaptic communication in 2 ways: they phosphorylate the existing AMPA receptors, thereby increasing AMPA conductance to sodium; and help to bring more AMPA receptors from intracellular stores to the post-synaptic membrane. This phase is thought to be the basis of short-term memory, which lasts for several hours. In the late phase, NEW proteins are made and gene expression is activated to further enhance the connection between the 2 neurons. These include newly synthesized AMPA receptors, and expression of other proteins that are involved in the growth of NEW dendritic spines and synaptic connections. The late phase may correlate with formation of long-term memory.

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Cardiac Action Potential, with Animation.

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The heart is essentially a muscle that contracts and pumps blood. It consists of specialized muscle cells called cardiac myocytes. The contraction of these cells is initiated by electrical impulses, known as action potentials. Unlike skeletal muscles, which have to be stimulated by the nervous system, the heart generates its OWN electrical stimulation. In fact, a heart can keep on beating even when taken out of the body. The nervous system can make the heartbeats go faster or slower, but cannot generate them. The impulses start from a small group of myocytes called the PACEMAKER cells, which constitute the cardiac conduction system. These are modified myocytes that lose the ability to contract and become specialized for initiating and conducting action potentials. The SA node is the primary pacemaker of the heart. It initiates all heartbeats and controls heart rate. If the SA node is damaged, other parts of the conduction system may take over this role. The cells of the SA node fire SPONTANEOUSLY, generating action potentials that spread though the contractile myocytes of the atria. The myocytes are connected by gap junctions, which form channels that allow ions to flow from one cell to another. This enables electrical coupling of neighboring cells. An action potential in one cell triggers another action potential in its neighbor and the signals propagate rapidly. The impulses reach the AV node, slow down a little to allow the atria to contract, then follow the conduction pathway  and spread though the ventricular myocytes. Action potential generation and conduction are essential for all myocytes to act in synchrony.

Pacemaker cells and contractile myocytes exhibit different forms of action potentials.

Cells are polarized, meaning there is an electrical voltage across the cell membrane. In a resting cell, the membrane voltage, known as the RESTING membrane potential, is usually negative. This means the cell is more NEGATIVE on the INSIDE. At this resting state, there are concentration gradients of several ions across the cell membrane: more sodium and calcium OUTSIDE the cell, and more potassium INSIDE the cell. These gradients are maintained by several pumps that bring sodium and calcium OUT, and potassium IN. An action potential is essentially a brief REVERSAL of electric polarity of the cell membrane and is produced by VOLTAGE-gated ion channels. These channels are passageways for ions in and out of the cell, and as their names suggest, are regulated by membrane voltage. They open at some values of membrane potential and close at others.

When membrane voltage INCREASES and becomes LESS negative, the cell is LESS polarized, and is said to be DE-polarized. Reversely, when membrane potential becomes MORE negative, the cell is RE-polarized. For an action potential to be generated, the membrane voltage must DE-polarize to a critical value called the THRESHOLD.

The pacemaker cells of the SA node SPONTANEOUSLY fire about 80 action potentials per minute, each of which sets off a heartbeat, resulting in an average heart rate of 80 beats per minute. Pacemaker cells do NOT have a TRUE RESTING potential. The voltage starts at about -60mV and SPONTANEOUSLY moves upward until it reaches the threshold of -40mV. This is due to action of so-called “FUNNY” currents present ONLY in pacemaker cells. Funny channels open when membrane voltage becomes lower than     -40mV and allow slow influx of sodium. The resulting DE-polarization is known as “pacemaker potential”. At threshold, calcium channels open, calcium ions flow into the cell further DE-polarizing the membrane. This results in the rising phase of the action potential. At the peak of depolarization, potassium channels open, calcium channels inactivate, potassium ions leave the cell and the voltage returns to -60mV. This corresponds to the falling phase of the action potential. The original ionic gradients are restored thanks to several ionic pumps, and the cycle starts over.

Electrical impulses from the SA node spread through the conduction system and to the contractile myocytes. These myocytes have a different set of ion channels. In addition, their sarcoplasmic reticulum, the SR, stores a large amount of calcium. They also contain myofibrils. The contractile cells have a stable resting potential of -90mV and depolarize ONLY when stimulated, usually by a neighboring myocyte. When a cell is DE-polarized, it has more sodium and calcium inside the cell. These positive ions leak through the gap junctions to the adjacent cell and bring the membrane voltage of this cell up to the threshold of -70mV. At threshold, FAST sodium channels open creating a rapid sodium influx and a sharp rise in voltage. This is the depolarizing phase. L-type, or SLOW, calcium channels also open at -40mV, causing a slow but steady influx. As the action potential nears its peak, sodium channels close quickly, voltage-gated potassium channels open and these result in a small decrease in membrane potential, known as EARLY RE-polarization phase. The calcium channels, however, remain open and the potassium efflux is eventually balanced by the calcium influx. This keeps the membrane potential relatively stable for about 200 msec resulting in the PLATEAU phase, characteristic of cardiac action potentials. Calcium is crucial in coupling electrical excitation to physical muscle contraction. The influx of calcium from the extracellular fluid, however, is NOT enough to induce contraction. Instead, it triggers a MUCH greater calcium release from the SR, in a process known as “calcium-induced calcium release”. Calcium THEN sets off muscle contraction by the same “sliding filament mechanism” described for skeletal muscle. The contraction starts about half way through the plateau phase and lasts till the end of this phase.

As calcium channels slowly close, potassium efflux predominates and membrane voltage returns to its resting value. Calcium is actively transported out of the cell and also back to the SR. The sodium/potassium pump then restores the ionic balance across the membrane.

Because of the plateau phase, cardiac muscle stays contracted longer than skeletal muscle. This is necessary for expulsion of blood from the heart chambers. The absolute refractory period is also much longer – 250 msec compared to 1 msec in skeletal muscle. This long refractory period is to make sure the muscle has relaxed before it can respond to a new stimulus and is essential in preventing summation and tetanus, which would stop the heart from beating.

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Ciclo de Puentes Cruzados – Contracción muscular, con Animación.

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La contracción muscular es la base de todos los movimientos esqueléticos. Los músculos esqueléticos se componen de fibras musculares, que a su vez están hechas de unidades funcionales repetitivas llamadas sarcómeros. Cada sarcómero contiene muchos filamentos paralelos y superpuestos delgados (actina) y gruesos (miosina). El músculo se contrae cuando estos filamentos se deslizan uno sobre el otro, resultando en un acortamiento del sarcómero y por lo tanto del músculo. Esto se conoce como la teoría de los filamentos deslizantes. El ciclo de puentes cruzados forma la base molecular para este movimiento de deslizamiento.

  • La contracción muscular inicia cuando las fibras musculares son estimuladas por un impulso nervioso y los iones de calcio son liberados.
  • Las unidades de troponina en los miofilamentos de actina son enlazadas a los iones de calcio. La unión desplaza la tropomiosina a lo largo de los miofilamentos y expone los sitios de unión a la miosina.
  • En esta etapa, cada cabeza de miosina está unida a un ADP y a una molécula de fosfato remanente del ciclo anterior.
  • Las cabezas de miosina se unen a los sitios de unión recién expuestos en los miofilamentos de actina para formar puentes cruzados y la molécula de fosfato es liberada.
  • Los dos miofilamentos se deslizan uno sobre el otro, impulsados por la energía química almacenada en las cabezas de miosina. A medida que avanzan, las moléculas de ADP son liberadas.
  • Los enlaces entre los miofilamentos de actina y las cabezas de miosina se rompen cuando las moléculas de ATP se unen a las cabezas de miosina.
  • Las moléculas de ATP son descompuestas en ADP y fosfato – la energía liberada por esta reacción es almacenada en las cabezas de miosina, lista para ser usada en el siguiente ciclo de movimiento.
  • Las cabezas de miosina reanudan sus posiciones de partida, y ahora pueden empezar una nueva secuencia de unión a la actina.
  • La presencia de más iones de calcio desencadenará un nuevo ciclo.
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Muscle Contraction – The Cross Bridge Cycle, with Animation.

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Muscle contraction is at the basis of all skeletal movements. Skeletal muscles are composed of muscles fibers which in turn are made of repetitive functional units called sarcomeres. Each sarcomere contains many parallel, overlapping thin (actin) and thick (myosin) filaments. The muscle contracts when these filaments slide past each other, resulting in a shortening of the sarcomere and thus the muscle. This is known as the sliding filament theory. Cross-bridge cycling forms the molecular basis for this sliding movement.
– Muscle contraction is initiated when muscle fibers are stimulated by a nerve impulse and calcium ions are released.
– To trigger muscular contraction, the troponin units on the actin myofilaments are bound by calcium ions. The binding displaces tropomyosin along the myofilaments, which in turn (and) exposes the myosin binding sites.
– At this stage, the head of each myosin unit is bound to an ADP and a phosphate molecule remaining from the previous muscular contraction.
– Now, the myosin heads release these phosphates and bind to the actin myofilaments via the newly exposed myosin binding sites.
– In this way, the actin and myosin myofilaments are cross-linked.
– The two myofilaments glide past one another, propelled by a head-first movement of the myosin units powered by the chemical energy stored in their heads. As the units move, they release the ADP molecules bound to their heads.
– The gliding motion is halted when ATP molecules bind to the myosin heads, thus severing the bonds between myosin and actin.
– The ATP molecules bound to myosin are now decomposed into ADP and phosphate, with the energy released by this reaction stored in the myosin heads, ready to be used in the next cycle of movement.
– Having been unbound from actin, the myosin heads resume their starting positions along the actin myofilament, and can now begin a new sequence of actin binding.
– Thus, the presence of further calcium ions will trigger a new contraction cycle

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What is CRISPR? How CRISPR Works, (with Animation)

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What is CRISPR?

CRISPR is the newly discovered REVOLUTIONARY tool that would allow scientists to change AT WILL any DNA sequence of, presumably, any living organism in a precise manner. Unlike any other previously developed techniques of gene editing, CRISPR is REMARKABLY simpler, faster and cheaper.

How CRISPR Works

CRISPR is part of a naturally occurring defense mechanism found in many bacteria. The bacteria use CRISPR to SPECIFICALLY snip the DNA of invading viruses. CRISPR stands for “Clustered Regularly Interspaced Short Palindromic Repeats” – a region of bacterial genome that contains short DNA repeats with unique sequences, or spacers, in between. These spacers are derived from DNA of viruses that prey on the bacteria. The CRISPR region is essentially a DNA library of all enemies that need to be RECOGNIZED and destroyed. After being transcribed, individual pieces of spacer RNAs form complexes with a protein named Cas, for CRISPR-ASsociated protein. Cas is an endonuclease – an enzyme that cuts DNA. These RNA/protein complexes then drift through the cell, looking for matching viral DNA. If a match is encountered, the RNA latches on, base-paring with it; Cas protein then cuts the viral DNA, disabling the virus.
Scientists have isolated this system, and by designing their own spacer-RNAs, they can, in theory, target any DNA sequences in any organism. The system has indeed worked in all organisms tested so far. The current CRISPR system consists of two components: a guide RNA and a Cas protein named Cas9. The guide RNA is a short synthetic RNA composed of a “scaffold” sequence necessary for Cas9-binding and a user-defined “spacer”, or “targeting” sequence of about 20 nucleotides long. One can change the genomic target of Cas9 by simply changing the targeting sequence present in the guide RNA. The entire system is designed in a plasmid that is subsequently used to transfect living cells.

Applications of the CRISPR System:

Disabling, or knock-out, a particular gene: After Cas-9 cuts the DNA, the cell would try to repair the break. The more efficient repair pathway in the cell is ERROR-PRONE and would most likely result in a loss-of-function mutation in the gene of interest. As CRISPR modifies BOTH copies of the gene at the same time, generation of knock-out animals and cell lines for gene function studies has never been more efficient. Moreover, MULTIPLE genes can be targeted in one manipulation, making this technique an extraordinarily powerful tool for studying complex genetic traits or diseases that involve many genes, such as cancers.
Introducing precise modifications to the target DNA: If a desired DNA sequence is provided together with the CRISPR/Cas-9 system, it can be used by ANOTHER repair pathway as a TEMPLATE to reconstruct the disrupted gene sequence. The desired changes will stay permanently and also transmitted to future generations. This can be used, for example, to swap a mutated copy of a gene with the good version, thereby restoring the gene’s function.
Regulating gene expression: Modifications to the Cas9 enzyme have extended the application of CRISPR to selectively turn ON and OFF target genes, fine-tune their expression WITHOUT permanently altering the gene sequence.
Since its discovery, CRISPR technology has been used extensively in animal research to engineer disease-resistant livestock; bring back extinct species; introduce deleterious genes into malaria-carrying mosquitoes; and modify pig genome to make pig’s organs suitable for transplant into human. Due to its relative simplicity, CRISPR has also been employed to create “custom designed” pets such as mini-pigs with customized coat patterns, colorful koi fish and dogs with certain desirable traits. The CRISPR zoo is growing rapidly but so are the ethical concerns and fears of possible ecological disasters.
In human, while CRISPR is proven to be a powerful tool to study various diseases, it is deemed NOT YET ready for clinical applications. This is because the Cas enzyme occasionally still cuts in the wrong place and hence cannot be used to introduce permanent changes to people. Modification of human germlines to alter genetic heritage of future generations may also lead to unwanted far-reaching consequences and is prohibited by most countries.

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Marijuana Effects on the Brain, the Goods and the Bads, with Animation Video.

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The Science of Marijuana

Marijuana, also known as cannabis, among other names, is a preparation of the Cannabis sativa plant – the hemp plant, intended for recreational and medicinal uses. Marijuana can be consumed by smoking, inhaling, or mixing with food.

The main psychoactive chemical in marijuana, responsible for most of the intoxicating effects sought by recreational users, is delta-9-tetrahydro-cannabinol, or THC. The Cannabis plant preparation also contains at least 65 other compounds that are chemically related to THC, called cannabinoids.

THC is chemically similar to a class of substances found naturally in our nervous system called endogenous cannabinoids, or endocannabinoids, of which anandamide is best known so far. The endocannabinoids are part of a newly discovered system named the Endocannabinoid system, or ECS.

How the ECS Works

A human brain contains billions of nerve cells, or neurons, which communicate via chemical messages, or neurotransmitters. When a neuron is sufficiently stimulated, a neurotransmitter is released into the synaptic cleft – a space between neurons. The neurotransmitter then binds to a receptor on a neighboring neuron, generating a signal in it, thereby transmitting the information to that neuron. Neuron communication is essential to all brain activities.

The ECS acts as a modulator of this neurotransmission. When the postsynaptic neuron is activated, endocannabinoids are produced, released, and travel back to the presynaptic neuron where they activate cannabinoid receptors. By doing so, they control what happens next when the presynaptic cell is again stimulated. The general effect is a DECREASE in the release of neurotransmitters such as GABA or glutamate. In other words, the ECS acts as a “brake”, SLOWING down neuronal activities, preventing neurons from excessive firing.

Some examples of ECS functions include:

 Pain modulation: cannabinoids SUPPRESS pain signal processing, producing pain relief effects.

 Stress and anxiety reduction: while response to stressful stimuli is necessary for an organism to react appropriately to a stressor, CHRONIC stress may be harmful. The ECS plays a role in the habituation of the body’s response to repeated exposure. It helps our body learn to restraint stress.

Mood regulation: the ECS promotes a “good feeling” by inducing dopamine release in the brain reward pathway. This explains the euphoria, or the “high”, experienced by marijuana users. THC mode of action is, however, different from other drugs: it induces dopamine release INDIRECTLY by removing inhibitory action of GABA on dopaminergic neurons.

The ECS is also involved in many other brain and bodily activities, including memory and learning, appetite and sleeping patterns, immune functions and fertility.

So how can marijuana be harmful if it does exactly what our body already does to itself?

The endocannabinoids are short-acting transmitter substances. They are synthesized on demand and their signaling is rapidly terminated by specific enzymes. The amount of endocannabinoid messengers is tightly regulated accordingly to the body’s needs. This regulation is essential for a modulator that acts to fine-tune brain activities.

Marijuana users consume a much higher amount of THC. THC is also much more stable than endocannabinoids and can persist in the body for a much longer period of time. THC overwhelms the endocannabinoid system, overriding normal brain functions. Because cannabinoid receptors are present in many parts of the brain and body, the effects of THC are wide-ranging. It can slow down a person’s reaction time, which could impair driving or athletic skills; disrupt short-term memory and higher thought processes, which could affect learning capabilities and judgment ability. Higher doses of THC may also lead to reverse effects. For example, while lower doses of cannabinoids seem to reduce stress, anxiety, and panic; higher doses may actually promote increased stressful feelings and fear. Consuming marijuana by smoking may also damage the lungs to a similar extent as smoking cigarettes.

Long – term Effects of THC

Substantial evidence from animal studies indicates that marijuana exposure can cause long-term adverse changes in the brain. Rats exposed to THC before birth, soon after birth, or during early life show significant difficulties with certain learning and memory tasks later in life. Long-term effects of marijuana in humans are still debatable mostly due to limitations of conducting research on human beings.

Medical Uses of Marijuana

While recreational use of marijuana is WITHOUT doubt harmful, the Cannabis plant may be a valuable source of medicines. Currently, the two main cannabinoids from the marijuana plant that are of medical interest are THC and cannabidiol, or CBD. These chemicals are used to increase appetite and reduce nausea in patients undergoing cancer chemotherapy. They may also be useful in reducing pain and inflammation, controlling epileptic seizures, and possibly even treating autoimmune diseases and cancers.

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Traducción Procariota, con Animación.

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Iniciación de la traducción en procariotas:
La subunidad pequeña del ribosoma se separa de la grande con la ayuda de dos factores de iniciación: IF1 e IF3. Este complejo se une entonces a una región rica en purinas – la secuencia Shine Dalgarno – aguas arriba del codón de inicio AUG en el ARN mensajero. La secuencia Shine Dalgarno es complementaria y está emparejada a una secuencia del ARN ribosómico 16S – un componente de la subunidad pequeña. Este alineamiento asegura que el codón de inicio se encuentra en la posición correcta dentro del ribosoma. Otro factor de iniciación – IF2 – lleva el ARN transferente iniciador cargado con el aminoácido de inicio N-formilmetionina. La subunidad grande del ribosoma se une al complejo y los factores de iniciación se liberan.
El ribosoma tiene tres sitios: el sitio A sirve de entrada a nuevos ARN transferentes cargados con aminoácidos o aminoacil-ARNt (aminoacil a erre ene te); el sitio P está ocupado por el peptidil-ARNt (peptidil a erre ene te) – el ARN transferente que lleva la cadena polipeptídica creciente; el sitio E es la salida de los ARN transferentes después de haber dejado el aminoácido. El ARN transferente iniciador se coloca en el sitio P.
Elongación: Un nuevo ARN transferente cargado entra en el sitio A del ribosoma. En el ribosoma, el anticodón del ARN transferente que llega se empareja con el codón del ARN mensajero que se encuentra en el sitio A. Durante esta revisión, los ARN transferentes con anticodones incorrectos se rechazan y se reemplazan por otros nuevos que también se revisarán. Cuando el aminoacil-ARNt (aminoacil a erre ene te) correcto entra al sitio A, se crea un enlace peptídico entre los ahora adyacentes aminoácidos. Conforme se forma en enlace peptídico, el ARN transferente del sitio P libera los aminoácidos al ARN transferente del sitio A y se queda vacío. Al mismo tiempo, el ribosoma se mueve un triplete hacia delante del ARN mensajero. Como consecuencia, el ARN transferente vacío se encuentra ahora en el sitio E y el peptidil-ARNt (peptidil a erre ene te) en el sitio P. El sitio A se encuentra ahora libre y listo para aceptar un nuevo ARN transferente. El ciclo se repite para cada codón del ARN mensajero.
Terminación: La terminación ocurre cuando en el sitio A se coloca alguno de los tres codones de parada. No hay ningún ARN transferente que pueda unirse al sitio A ya que ninguno puede emparejarse con esa secuencia. En su lugar, estos codones son reconocidos por una proteína, un factor de terminación. Al unirse este factor de terminación se cataliza la escisión del enlace que une el polipéptido y el ARN transferente. El polipéptido se libera del ribosoma. El ribosoma se disocia en sus subunidades y está listo para un nuevo ciclo de traducción.

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Traducción Eucariota – Síntesis de Proteínas, con Animación.

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Pasos del proceso de traducción:
Iniciación: La subunidad pequeña del ribosoma se une al ARN transferente iniciador que lleva el aminoácido de inicio Metionina. Este complejo se une entonces a la estructura CAP del extremo 5 prima del ARN mensajero y lo escanea hasta encontrar el codón de inicio AUG. El proceso está mediado por varios factores de iniciación. En el codón de inicio, la subunidad grande del ribosoma se une a todo el complejo y los factores de iniciación se liberan.
El ribosoma tiene tres sitios: el sitio A sirve de entrada a nuevos ARN transferentes cargados con aminoácidos o aminoacil-ARNt (aminoacil a erre ene te); el sitio P está ocupado por el peptidil-ARNt (peptidil a erre ene te) – el ARN transferente que lleva la cadena polipeptídica creciente; el sitio E es la salida de los ARN transferentes después de haber dejado el aminoácido. El ARN transferente iniciador se coloca en el sitio P.
Elongación: Un nuevo ARN transferente cargado entra en el sitio A del ribosoma. En el ribosoma, el anticodón del ARN transferente que llega se empareja con el codón del ARN mensajero que se encuentra en el sitio A. Durante esta revisión, los ARN transferentes con anticodones incorrectos se rechazan y se reemplazan por otros nuevos que también se revisarán. Cuando el aminoacil-ARNt (aminoacil a erre ene te) correcto entra al sitio A, se crea un enlace peptídico entre los ahora adyacentes aminoácidos. Conforme se forma en enlace peptídico, el ARN transferente del sitio P libera los aminoácidos al ARN transferente del sitio A y se queda vacío. Al mismo tiempo, el ribosoma se mueve un triplete hacia delante del ARN mensajero. Como consecuencia, el ARN transferente vacío se encuentra ahora en el sitio E y el peptidil-ARNt (peptidil a erre ene te) en el sitio P. El sitio A se encuentra ahora libre y listo para aceptar un nuevo ARN transferente. El ciclo se repite para cada codón del ARN mensajero.
Terminación: La terminación ocurre cuando en el sitio A se coloca alguno de los tres codones de parada. No hay ningún ARN transferente que pueda unirse al sitio A ya que ninguno puede emparejarse con esa secuencia. En su lugar, estos codones son reconocidos por una proteína, un factor de terminación. Al unirse este factor de terminación se cataliza la escisión del enlace que une el polipéptido y el ARN transferente. El polipéptido se libera del ribosoma. El ribosoma se disocia en sus subunidades y está listo para un nuevo ciclo de traducción.
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Mecanismo da Dependência Química no Cérebro, com Animação.

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A dependência química é uma desordem neurológica que afeta o sistema de recompensa no cérebro. Em uma pessoa saudável, o sistema de recompensa reforça comportamentos que são essenciais para a sobrevivência, como: comer, beber, comportamento sexual e interação social. Por exemplo, o sistema de recompensa garante que você busque comida quando está com fome, porque você sabe que depois de comer se sentirá bem. Em outras palavras, ele torna a atividade de comer agradável e memorável, para que você queira fazer isso sempre que sentir fome. Drogas de abuso se apropriam desse sistema, tornando as necessidades naturais da pessoa em necessidade de drogas.
O cérebro é composto por bilhões de neurônios, ou células nervosas, que se comunicam através de mensageiros químicos ou neurotransmissores. Quando um neurônio é estimulado o suficiente, um impulso elétrico, chamado de potencial de ação, é gerado e viaja ao longo do axônio para a terminação nervosa. Aqui, é desencadeada a liberação de um neurotransmissor na fenda sináptica – um espaço entre os neurônios. O neurotransmissor, em seguida, se liga no receptor do neurônio vizinho, gerando um sinal nele, transmitindo, assim, a informação para esse neurônio.
As principais vias de recompensa envolvem a transmissão do neurotransmissor DOPAMINA, a partir da área tegmental ventral, a ATV, do mesencéfalo para o sistema límbico e para o córtex frontal. Participar de atividades agradáveis gera potenciais de ação em neurônios produtores de dopamina no ATV. Isso faz com que haja a liberação de dopamina pelos neurônios na fenda sináptica. Em seguida, a dopamina se liga e estimula o receptor de dopamina no neurônio pós-sináptico. Acredita-se que essa estimulação pela dopamina produza sensações de prazer ou efeito de recompensa. Moléculas de dopamina são, em seguida, removidas da fenda sináptica e transportadas de volta para o neurônio transmissor por uma proteína especial, chamada de transportador de dopamina.
A maioria das drogas de abuso AUMENTAM a concentração de dopamina na via de recompensa. Algumas drogas, como o álcool, heroína e nicotina estimulam os neurônios produtores de dopamina indiretamente na ATV para que eles gerem mais potenciais de ação. A cocaína atua na terminação nervosa. Ela liga-se ao transportador de dopamina e bloqueia a recaptação de dopamina. Metanfetamina – um estimulante – atua de forma semelhante à cocaína no bloqueio da remoção de dopamina. Além disso, ela pode entrar no neurônio, nas vesículas que contêm dopamina, provocando a liberação de dopamina, mesmo na ausência de potenciais de ação.
Diferentes drogas agem de maneira diferente, mas o resultado comum é que a dopamina se acumula na sinapse em uma quantidade MUITO MAIOR do que a normal. Isso provoca uma estimulação contínua, talvez, a super estimulação dos neurônios pós-sinápticos seja responsável pela euforia prolongada e intensa, experimentada por usuários de drogas. Exposições repetidas a surtos de dopamina, causados pelas drogas, eventualmente DESSENSIBILIZAM o sistema de recompensa. O sistema deixa de responder a estímulos cotidianos; a única coisa que se torna gratificante é a droga. Dessa maneira, as drogas alteram as prioridades da vida da pessoa. Depois de algum tempo, até mesmo a droga perde a sua capacidade de recompensa e as doses necessárias para atingir o efeito de recompensa são mais elevadas, levando a overdose de drogas.

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