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In laboratory mice that are raised to be completely free of bacteria arteria carotis communis discount metoprolol 100 mg free shipping, the mouse norovirus can substitute for bacteria in some of these roles. Some structural details can be seen, but the virus typically has a poorly defined structural appearance. Water-borne cause of infantile paralysis A pathogen that resists eradication Poliovirus is one of the most well-studied viruses; many landmarks in molecular virology were developed with polio. Although Poliovirus has probably infected humans since ancient times, poliomyelitis, or infantile paralysis was very rare until the twentieth century. This is likely because people recognized that diseases could be carried in water, and water supplies were decontaminated with filtration or chemicals such as chlorine. Before this, most children contracted polio when they were very young, and in infants the virus rarely causes any noticeable symptoms. Although water was cleaned up, sewage treatment was not widespread until the 1960s and 1970s, so exposure to polio still occurred, but from sources other than drinking water. When people first acquired polio at later stages of childhood, poliomyelitis became more common. Roosevelt contracted polio in 1921 and remained in a wheelchair for the rest of his life. When he became the 32nd president of the United States he started a "war on polio," and began the Foundation for Infantile Paralysis, now the March of Dimes. The polio vaccine changed the face of the disease; introduced as a heat-killed virus vaccine in 1954, widespread vaccination began in 1962 when an attenuated vaccine was introduced that could be given in sugar cubes. This form is used throughout much of the world today, although the heat-killed vaccine is used in developed countries. The attenuated strain in the live vaccine can, very rarely, escape and cause poliomyelitis. The geometric structure of polio is typically less defined than for some other small icosahedral viruses (for example see Human adenovirus). The feces of an infected person can contain up to ten trillion particles per gram, and only ten are required for infection. The virus is stable to normal methods for sanitizing water, so it is hard to control. Although Rotavirus infection can occur at any age, disease mostly occurs in children, and childhood infection usually results in some immunity. Subsequent infections, if they occur, are usually without symptoms, and strengthen immunity against further infection. In the developed world vaccination controls much of the problem, but in other parts of the world Rotavirus is common. It is especially problematic when children have other conditions, such as malnutrition or other infectious diseases. In some cases outbreaks are due to mutations in the virus, making it resistant to the immunity of a population. If a chance mutation allows a virus to escape the host immune system it will have an advantage over other individual viruses, and can rapidly become the dominant strain. Rotavirus diarrhea is similar to many other childhood illnesses, and requires a laboratory test to determine the cause. In otherwise healthy children the disease is usually resolved in three to seven days, and treatment includes keeping children hydrated. The disease was severe, and fatality rates ranged from 10 percent in otherwise healthy adults, to more than 50 percent in the elderly. Molecular evidence indicates that the virus originated in bats, then either moved to civets (a wild cat in China), and then to humans, or from bats to humans to civet cats. The worldwide spread was due to infected travelers, and encompassed 32 countries in less than three months. The public health and virology communities reacted rapidly; within about six months the entire sequence of the virus was determined, and a few months later a complex set of tools for studying the virus was developed. Surveillance for infected travelers was also prompt, and travel through some large airports in China and other parts of the world involved detecting persons with elevated temperatures. By April of 2004 a vaccine was being tested in mice, but there were no additional natural human cases reported after January of 2004, although a few laboratory cases occurred in China and Taiwan.

In this first clinical case study arteria carotis communis 50 mg metoprolol order with visa, we examine a serious and potentially lifethreatening condition that can occur in individuals in whom body temperature homeostasis is disrupted. All of the material presented in this clinical case study will be explored in depth in subsequent chapters, as you learn the mechanisms that underlie the pathologies and compensatory responses illustrated here in brief. Notice as you read that the first two general principles of physiology described earlier are particularly relevant to this case. It is highly recommended that you return to this case study as a benchmark at the end of your semester; we are certain that you will be amazed at how your understanding of physiology has grown in that time. A 64-year-old, fair-skinned man in good overall health spent a very hot, humid summer day gardening in his backyard. After several hours in the sun, he began to feel light-headed and confused as he knelt over his vegetable garden. Although earlier he had been perspiring profusely and appeared flushed, his sweating had eventually stopped. Because he also felt confused and disoriented, he could not recall for how long he had not been perspiring, or even how long it had been since he had taken a drink of water. He called to his wife, who was alarmed to see that his skin had since turned a pale-blue color. She asked her husband to come indoors, but he fainted as soon as he tried to stand. The wife called for an ambulance, and the man was taken to a hospital and diagnosed with a condition called heatstroke. Based on that, what would you expect to occur to skin blood vessels when a person first starts feeling warm As you learned in this chapter, body temperature is a physiological function that is under homeostatic control. Conversely, as in our example here, if body temperature increases, heat production decreases and heat loss increases. When our patient began gardening on a hot, humid day, his body temperature began to increase. At first, the blood vessels in his skin dilated, making him appear flushed and helping him dissipate heat across his skin. To understand this, we must consider that several homeostatic variables were disrupted by his activities. As the sweating continued, it resulted in decreased fluid levels and a negative balance of key ion concentrations in his body; this contributed to a decrease in mental function, and he became confused. As his body fluid levels continued to decrease, his blood pressure also decreased, further endangering brain function. Though it is potentially life threatening for body temperature to increase too much, it is also life threatening for blood pressure to decrease too much. Eventually, many of the blood vessels in regions of the body that are not immediately required for survival, such as the skin, began to constrict, or close off. By doing so, the more vital organs of the body-such as the brain-could receive sufficient blood. It also made it more difficult for sweat glands in the skin to obtain the fluid required to produce sweat. The man gradually decreased perspiring and eventually stopped sweating altogether. This case illustrates a critical feature of homeostasis that you will encounter throughout this textbook and that was emphasized in this chapter. Often, when one physiological variable such as body temperature is disrupted, the compensatory responses initiated to correct that disruption cause, in turn, imbalances in other variables. These secondary imbalances must also be compensated for, and the significance of each imbalance must be "weighed" against the others. In this example, the man was treated with intravenous fluids made up of a salt solution to restore his fluid levels and concentrations, and he was immersed in a cool bath and given cool compresses to help reduce his body temperature. Although he recovered, many people do not survive heatstroke because of its profound impact on homeostasis. Efferent pathways carry information away from the integrating center of a reflex arc. In a reflex arc initiated by touching a hand to a hot stove, the effector belongs to which class of tissue The type of tissue involved in many types of transport processes, and which often lines the inner surfaces of tubular structures, is called.

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This organ consist s of a system of sensory cells and supporting cells covered by an acellular gelatinous ap hypertensive disorder 50 mg metoprolol order with visa, the tectorial membrane. The sensory cells (inner and outer hair cells) are the receptors of the organ of Corti (c). These cells bear approxim ately 50­100 stereocilia, and on their apical surface synapse on their basal side with the endings of a erent and e erent neurons. They have the abilit y to transform m echanical energy into electrochem ical potentials (see below). A m agni ed cross-sectional view of a cochlear turn (c) also reveals the stria vascularis, a layer of vascularized epithelium in which the endolymph is form ed. This endolymph lls the m em branous labyrinth (appearing here as the cochlear duct, which is part of the labyrinth). It transform s the energy of the acoustic traveling wave into electrical im pulses, which are then carried to the brain by the cochlear nerve. The function of the basilar m em brane is to transm it acoustic waves to the inner hair cell, which transform s them into impulses that are received and relayed by the cochlear ganglion. The sound pressure induces m otion of the oval window m em brane, whose vibrations are in turn, transm it ted through the perilymph to the basilar m em brane of the inner ear (see b). These are the sites where the receptors of the organ of Corti are stim ulated and signal transduction occurs. To understand this process, one m ust rst grasp the structure of the organ of Corti (the actual organ of hearing), which is depicted in C. In response, the hair cells actively change their length, thereby increasing the local am plitude of the traveling wave. This additionally bends the stereocilia of the inner hair cells, stim ulating the release of glutam ate at their basal pole. The release of this substance generates an excitatory potential on the a erent nerve bers, which is transm it ted to the brain. It consists of the m em branous sem icircular duct s, which contain sensory ridges (am pullary crests) in their dilated portions (ampullae), and of the saccule and utricle with their m acular organs (their location in the petrous bone is shown in B, p. The sensory organs in the sem icircular duct s respond to angular acceleration while the m acular organs, which have an approxim ately vertical and horizontal orientation, respond to horizontal (utricular m acula) and vertical (saccular m acula) linear acceleration, as well as to gravitational forces. B Structure of the ampulla and ampullary crest Cross-section through the ampulla of a sem icircular canal. Each canal has a bulbous expansion at one end (ampulla) that is traversed by a connective tissue ridge with sensory epithelium (ampullary crest). Extending above the ampullary crest is a gelatinous cupula, which is at tached to the roof of the ampulla. Each of the sensory cells of the ampullary crest (approxim ately 7000 in all) exhibit s one long kinocilium and approxim ately 80 shorter stereocilia on their apical pole, which project into the cupula. When the head is rotated in the plane of a particular sem icircular canal, the inertial lag of the endolymph causes a de ection of the cupula, which in turn causes a bowing of the stereocilia. The sensory cells are either depolarized (excitation) or hyperpolarized (inhibition), depending on the direction of ciliary displacem ent (see details in E). Anterior sem icircular canal Anterior sem icircular duct Ampullary crest with lateral ampullary nerve Endolymphatic sac Lateral sem icircular duct Posterior sem icircular duct Ampullary crest with anterior ampullary nerve Vestibular ganglion, superior part Vestibular ganglion, inferior part Utricle Utricular m acula with utricular nerve Saccular m acula with saccular nerve Saccule Endolymphatic duct Ampullary crest with posterior ampullary nerve Ductus reuniens Sem icircular canal Am pulla Cupula Cilia of sensory cells Supporting cell Sensory cell C Structure of the utricular and saccular maculae the m aculae are thickened oval areas in the epithelial lining of the utricle and saccule, each averaging 2 m m in diam eter and containing arrays of sensory and supporting cells. Like the sensory cells of the am pullary crest, those of the m acular organs bear specialized stereocilia, which project into an otolithic m em brane. The lat ter consist s of a gelatinous layer, sim ilar to the cupula, but it has calcium carbonate crystals or otoliths (statoliths) em bedded in its surface. With their high speci c gravit y, these crystals exert traction on the gelatinous m ass in response to linear acceleration, and this induces shearing m ovem ent s of the cilia. The sensory cells are either depolarized or hyperpolarized by the m ovem ent, depending on the orientation of the cilia. Orga ns and Their Neurovascula r Structures Stereocilia Kinocilium Sensory cell Tim e Afferent nerve fiber D Stimulus transduction in the vestibular sensory cells Each of the sensory cells of the m aculae and am pullary crest bears on it s apical surface one long kinocilium and approxim ately 80 stereocilia of graduated lengths, form ing an array that resem bles a pipe organ. When the stereocilia are de ected toward the kinocilium, the sensory cell depolarizes and the frequency of action potentials (discharge rate of impulses) is increased (right side of diagram). When the stereocilia are de ected away from the kinocilium, the cell hyperpolarizes and the discharge rate is decreased (left side of diagram).

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Axons of the second neurons can also ascend to the reticular formation (spinoreticular bers) or to the mesencephalon (spinomesencephalic bers) for the subcortical processing of painful stim uli heart attack 22 generic 50 mg metoprolol visa. These axons rem ain uncrossed and travel in the lateral funiculus of the spinal cord to the ipsilateral brainstem. The cell bodies of the second neurons that form the anterior spinocerebellar tract are located in the middle of the ipsilateral posterior horn. Their axons run in the lateral funiculus either crossed (at the anterior white com missure) or uncrossed and reach the brainstem. The axons of the posterior spinocerebellar tract travel via the inferior cerebellar peduncle to the ipsilateral cerebellum. The axons of the anterior spinocerebellar tract reach the m esencephalon and then the cerebellum through the superior cerebellar peduncle. The bers in this tract that crossed in the spinal cord, cross back to their original side. The axons of the second neurons travel uncrossed through the ipsilateral inferior cerebellar peduncle to the cerebellum. Sim ilar to posterior spinocerebellar tract, collaterals from the cuneocerebellar tract project to the thalam us, which in turn project s to the telencephalon (ensuring conscious proprioception for the upper body). Their axons travel to the cerebral cortex (to the fourth neurons) in the thalam ic radiations in the posterior lim b of the internal capsule. In case of the spinothalam ic pathway, bodies of fourth neurons are also located in the cingulate gyrus. Soma totopic orga niza tion of tra cts Fibers corresponding to the sacral spinal segm ent s are located m edial or dorsal, while those corresponding to the cervical segm ent s are positioned lateral or ventral. Symptoms · Dysfunction of fasciculus gracilis leads to impaired epicritic perception. A rough classi cation based on their functions, which is still used in the clinic, is analogous to the tract s, as one refers to pyram idal and extrapyram idal m otor functions. Pyra mida l bers in the spina l cord (Anterior a nd la tera l corticospina l tra cts) De nition and function: · Major m otor tract (voluntary m otor function, conscious m ovem ent control of neck, trunk and lim bs) · the part of the pyramidal tract, which extends from the prim ary m otor cortex to the spinal cord. Only when it reaches the spinal cord, is it called corticospinal tract; before entering the spinal cord, the bers of this descending tract are usually referred to as corticospinal bers. Like the other bers of the pyram idal tract (bers in the corticobulbar tract to the cranial nerve nuclei and corticoreticular bers to the reticular form ation), they include axons of the large pyram idal cells. On functional grounds, they are considered in the sam e category as the corticospinal bers and based on their neurons of origin, they are usually considered part of the "pyram idal bers. From there ­ the uncrossed 20% run ipsilaterally in the spinal cord as the anterior corticospinal tract; they cross in the anterior white com m issure only at the level of the spinal segm ent where those bers end. Lower motor neuron: - or -m otor neurons in the anterior horn of the spinal cord, largely in the lam inae A-C after Rexed, on which the axons of the corticospinal tract term inate. Axons of the lower m otor neuron end on target organs, in this case striate m uscles. The axons of the lower m otor neurons form the som atom otor fibers in the composition of the spinal nerve. Upper motor neuron: Large pyram idal cells in the internal pyram idal layer (layer V) of the precentral gyrus (prim ary m otor cortex); 40% of which are located in the Brodm an area 4; the rem aining 60% are located in neighboring brain regions. Course of the axons of the upper m otor neurons: On their descending way from the telencephalon, to the decussation of the pyram ids the corticospinal bers travel through the · Prim ary m otor cortex posterior lim b of the internal cap sule, cerebral peduncles of the m idbrain base of the pons (basal pons) m edullary pyram id Extra pyra mida l bers in the spina l cord De nition and function: Major motor pathways (mainly for ne movement control). The extrapyram idal pathways originate as upper m otor neurons in brainstem nuclei and the prem otor cortex, end m ostly on -m otor neurons in the spinal cord (as lower m otor neurons), and are usually collectively called "extrapyram idal m otor" pathways. They are responsible for ne-tuning m otor function and subcortical preparation of a cortically initiated m ovem ent. Major extrapyramidal pathw ays are as follow s: · Lateral/ Medial vestibulospinal tracts: originate in the vestibular · · · · nuclei. Ponto- and m edullary reticulospinal tract s: originate in the reticular form ation nuclei of the pons and m edulla oblongata respectively Rubrospinal tract: originates in the red nucleus. Soma totopic orga niza tion of the a nterior a nd la tera l corticospina l tra cts (not known for extrapyram idal pathways in hum ans) · In the posterior lim b of the internal capsule: cervical bers rostral; sacral bers occiptial · In the cerebral peduncles (m idbrain): cervical bers m edial; sacral bers lateral · In the spinal cord: cervical bers m edial; sacral bers lateral Symptoms Dysfunction of the corticospinal tract leads to impaired voluntary m ovem ent of the neck, trunk, and lim bs. Depending on the extent of the dam age, it can result in paresis (loss of crude voluntary m ovem ent) or plegia (complete paralysis) of m uscles or m uscle groups. Since dam age of the corticospinal bers or tract as a result of the m echanism of injury.

Usage: p.c.

If the brain is cut horizontally at the border bet ween telencephalon and diencephalon hypertension case study order metoprolol 50 mg without prescription, all basal nuclei are visible. The sm all globus pallidus is located m edially to the putam en (thus not visible in the lateral view, see B). The internal capsule, a boom erang-shaped area of white m at ter, which contains ascending and descending projection tracts, is surrounded by basal nuclei and the thalam us (see A, p. The anterior lim b of the internal capsule, runs bet ween the head of the caudate nucleus and lentiform nucleus; the genu, and the posterior lim b are located between the thalam us and the lentinform nucleus, thus at the border between telencephalon and diencephalon. Note: Lateral to the putam en, directly m edial to the insular cortex, lies a nucleus that is referred to as claustrum (front wall). The claustrum is not a basal nucleus (though it once was referred to as one); it s function is largely unknown; it is believed to be involved in regulating sexual behavior. The coronal section that was chosen here, cut s though the head of the caudate nucleus, which protrudes into the anterior horn of the lateral ventricle. The anterior lim b of the internal capsule passes bet ween the basal nuclei, which are located close to one another, and due to the alternating arrangem ent of gray and white m at ter gives the gray m at ter of the nuclei a striated appearance (corpus striatum). The coronal section (b) illustrates the close topographical relationship bet ween the caudate nucleus and the corpus callosum, which in this im age is located supero-m edial to the caudate nucleus and form s the roof of the lateral ventricle. The diencephalon is located beneath the t wo cerebral hem ispheres and above the brainstem. The anterior, superior, and lateral part s of the diencepahlon directly adjoint the telencephalon. The posterior part of the base is located at the poorly de ned border with the m esencephalon, the anterior part- ned by the hypothalam us- de has been exposed. The third ventricle located in the m edian plane divides the diencephalon into sym m etrical halves which either contain paired structures (in the lateral wall of the third ventricle. As a result of the position of the individual part s of the diencepahlon, the third ventricle has several extensions, or recesses. The corpus callosum and the septum pellucidum (the partition bet ween the lateral ventricles) are clearly visible and therefore helpful anatom ical reference points. Lo- cated beneath the corpus callosum, the thalam us occupies the largest area of the lateral wall of the third ventricle. Due to it s projection into the ventricular lum en, the third ventricle is separated from the sm ooth wall of the hypothalam us by a furrow: the hypothalam ic sulcus. The fornix (arch) is an arch-shaped structure that passes above the thalam us and surrounds it. It extends bet ween the (hippocampus which is part of the telencephalon) and the m am m illary bodies. As a projection tract, it is, topographically and functionally, part of both the telencepahlon and the diencephalon. Topographically, the fornix is occasionally referred to as the roof of the third ventricle. Note: One part of the diencephalon, which is particularly im portant for m otor functions, the subthalam us, due to it s far lateral location, can never be seen on the m idsagit tal section but only on coronal (see B, p. Diencepha lon Telencephalic vesicle Diencephalic vesicle Mesencephalic (m idbrain) vesicle Rhom bencephalic vesicle Choroid plexus Lateral ventricle Diencephalon Tela choroidea a Corpus callosum Caudate nucleus Diencephalon Telencephalon Choroid plexus Telodiencephalic boundary Portion of diencephalon visible at the base of the brain Tela choroidea Fornix Third ventricle b Mam m illary body (diencephalon) B Development of the diencephalon from the cranial neural tube Anterior view. To understand the location and extent of the diencephalon in the adult brain, it is necessary to know how it develops from the neural tube. The diencephalon and telencephalon both develop from the prosencephalon, or forebrain (see p. As developm ent proceeds, the t wo hem ispheres of the telencephalic vesicle (red) expand, overgrowing the diencephalic vesicle (blue). This process shifts the boundary bet ween the telencephalon and diencephalon until only a sm all area of the diencephalon can be seen at the base of the developed brain (see A). The developm ent of the telencephalon (red) has progressed considerably in relation to B.

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