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storchak [24]
3 years ago
15

How are dendrites synthesized in a neuron?

Medicine
1 answer:
hram777 [196]3 years ago
7 0

Answer:

The processing power of the mammalian brain is derived from the tremendous interconnectivity of its neurons. An individual neuron can have several thousand synaptic connections. While these associations yield computational power, it is the modification of these synapses that gives rise to the brain's capacity to learn, remember and even recover function after injury. Inter-connectivity and plasticity come at the price of increased complexity as small groups of synapses are strengthened and weakened independently of one another (Fig. 1). When one considers that new protein synthesis is required for the long-term maintenance of these changes, the delivery of new proteins to the synapses where they are needed poses an interesting problem (Fig. 1). Traditionally, it has been thought that the new proteins are synthesized in the cell body of the neuron and then shipped to where they are needed. Delivering proteins from the cell body to the modified synapses, but not the unmodified ones, is a difficult task. Recent studies suggest a simpler solution: dendrites themselves are capable of synthesizing proteins. Thus, proteins could be produced locally, at or near the synapses where they are needed. This is an elegant way to achieve the synapse specific delivery of newly synthesized proteins.

Explanation:

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Answer:

The answer for the question is B

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Un paciente masculino presenta insuficiencia hepática crónica puede presentar trastornos hemostásicos. Explique y razone su resp
pychu [463]
La insuficiencia hepática es un estado patológico que condiciona la síntesis y metabolismo de diversas biomoléculas, siendo las alteraciones a la hemostasia una de las primeras consecuencias a nivel sistémico que se hacen presentes; debido a esto y por la dimensión de los riesgos de esta situación, no es raro que las pruebas de coagulación sean indispensables para formular las escalas pronósticas en pacientes hepatópatas.

La cascada de activación de los factores de la coagulación ha sido perfeccionada hasta conformarse el ahora vigente modelo celular que considera la valiosa e indispensable participación del endotelio y las plaquetas.

En la enfermedad hepática existe una acumulación masiva de lípidos en el hepatocito que inducen la liberación de diversos mediadores inflamatorios, entre los que se pueden mencionar la interleucina (IL) 1 y 6, el factor de necrosis tumoral (TNF) y la estimulación del receptor LPS/Toll-like (TLR-4) presentes en las células de Kupffer Estas vías desencadenan una disregu- lación del endotelio mediante la activación de la dimetilar- ginina asimétrica (ADMA), un inhibidor endógeno de la óxido nítrico sintetasa (eNOS)


La mayor parte de los factores procoagulantes como el fibrinógeno, la protrombina y los factores V, VII, IX, X, XI y XII son de síntesis hepática, por lo que sus niveles séricos se modifican en relación con el grado de daño hepático. Los factores V y VIII son los primeros en disminuir por poseer las vidas medias más cortas (12 y 4-6 horas, respecti- vamente). Es común que los pacientes cirróticos sufran reducciones moderadas del factor VII, identificándose una relación significativa entre los niveles de factor VII y el tiempo de protrombina (TP)

Cuando se evalúan las pruebas de coagulación en pacien- tes con hepatopatías, es importante descartar defectos con- génitos; el más frecuente es la deficiencia de factor VII. Esta deficiencia congénita se ha descrito en varias entidades clínicas (embarazo, cardiopatía, enfermedad pulmonar obstructiva, entre otras), aunque se tienen registrados pocos casos en px cirróticos.

Gracias a esto es posible comprender que, en pacientes con insuficiencia hepática, el riesgo de sangrado no obedece únicamente a la deficiencia en la producción de los factores de la coagulación y, por tanto, es cuestionable la administración de vitamina K.

6 0
3 years ago
Which independent nursing action would be included in the plan of care for a client after an episode of ketoacidosis
agasfer [191]

Answer:

Monitoring for signs of hypoglycemia as a result of treatment

Explanation:

3 0
3 years ago
Read 2 more answers
A football player comes into the athletic training room with the help of a couple of teammates. He explains that he twisted his
Sliva [168]

Answer:

It could be a fractured knee or out of place

Explanation:

His leg felt like giving out when attempting to walk. He explains that he twisted his knee while trying to change direction. He heard a loud pop as his knee gave in.

5 0
4 years ago
Describe how the tibial collateral ligament could be damaged if the knee is impacted on the lateral surface.
zhannawk [14.2K]

Answer:

the tibial collateral ligament can be damaged when the knee is impacted on lateral surface -

Sprain is mild stretch or tear , Sprain is partial tear and Sprain is full tear of the ligament .

Explanation:

Tibial Collateral ligament

Tibial Collateral ligament is one of the four important ligaments in knee. It joins femur with tibia or shinbone. The kneecap sits in the middle of this joint. Ligaments are very sensitive to strains. Tibial collateral ligament is most common ligament to get damage, specially for athletes. There could be three form of injury to this ligament.

Grade 1

Sprain is mild stretch or tear,

Grade 2

Sprain is partial tear and

Grade 3

Sprain is full tear of the ligament.

The damage occurs due to sudden force which is extensive for the ligament and it overstretches. Sudden impact on lateral surface will push the knee sideways, giving stress on the ligament, making it overstretch; and if the force is too great ligament will tear.

7 0
3 years ago
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