scholarly journals MULTIPLICATION AND SPREAD OF THE VIRUS OF ST. LOUIS ENCEPHALITIS IN MICE WITH SPECIAL EMPHASIS ON ITS FATE IN THE ALIMENTARY TRACT

1947 ◽  
Vol 85 (6) ◽  
pp. 647-662 ◽  
Author(s):  
John L. Peck ◽  
Albert B. Sabin
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intestinal Tract ◽  
Antiviral Agent ◽  
Nerve Fibers ◽  
Human Beings ◽  
Poliomyelitis Virus ◽  
Virus Content ◽  
The Central Nervous System ◽  
The Brain

1. Beginning at 24 hours after intravenous injection of about 10 million intracerebral LD50 of virus there was evidence of simultaneous, progressive multiplication in the brain and intestinal tract. 2. When the virus was introduced directly into the brain or the nasal cavities and mouth, none was found in the intestinal tract until there was general centrifugal spread from the central nervous system during the last stages of the infection at 96 or 120 hours after inoculation when the virus in the entire brain had reached a concentration of about 3 billion LD50. 3. Centrifugal spread began when the virus in the brain reached a concentration of about 400 million LD50 and virus appeared in the pharynx, tongue, and adrenals before it was demonstrable in the intestinal tract, blood, or viscera such as the spleen, liver, and kidneys. 4. Despite the high concentrations of virus which developed in the intestinal tract following intravenous inoculation, it was not demonstrable in the stools, differing in this respect from Theiler's virus in mice and poliomyelitis virus in human beings and monkeys. 5. No antiviral agent was found in the stools, but the urine of normal mice having a pH of 5.6, inactivated large amounts of St. Louis encephalitis virus. 6. There was no evidence of multiplication in the nasal mucosa of mice which succumbed with encephalitis following nasal instillation of the virus, the course of events being comparable in this respect to the behavior of the M.V. poliomyelitis virus in rhesus monkeys. 7. At the terminal stage of infection the virus content per milligram of tissue was as great in the leg muscles as in the sciatic nerves. Since this was also true for the urinary bladder, heart, lungs, and tongue among other tissues, and since the amount in the blood was too negligible to account for it, it would appear that the virus either accumulated in these tissues by diffusion from the nerve fibers, along which it was spreading from the central nervous system, or that it multiplied in some constituent other than the nerve fibers.

A Suspected New Storage Disease in Cattle

1982 ◽  
Vol 19 (6) ◽  
pp. 616-622 ◽  
Author(s):  
W. J. Hartley ◽  
R. F. Webb
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Brain Stem ◽  
Storage Disease ◽  
Nerve Fibers ◽  
Myelinated Nerve ◽  
Myelinated Nerve Fibers ◽  
The Central Nervous System ◽  
Motor Columns ◽  
The Brain

A suspected storage disease occurred in 50% of a group of five- to seven-month-old Hereford calves in one of four years following the same mating procedure. Lesions were confined to the central nervous system and consisted of multiple intraneuronal, cytoplasmic laminated cytosomes in restricted areas of the brain stem, together with extensive loss of myelinated nerve fibers in the motor columns of the cord.

scholarly journals About ascending degenerations in the brainstem and descending in the spinal cord (after damage to the lateral part of the brain between the occipital foramen and atlant)

2020 ◽  
Vol VI (1) ◽  
pp. 92-117
Author(s):  
S. A. Sukhanov
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Nervous Tissue ◽  
Nerve Fibers ◽  
Lateral Part ◽  
The Central Nervous System ◽  
The Brain ◽  
Occipital Foramen

Among the new ways of coloring the nervous tissue, which gave us a lot of new facts and partly contributing to the changes in our previous information about the course of fibers in the central nervous system, is the Marchi method, which is very common at the present time, due to its extreme convenience and simplicity in defining degeneration nerve fibers.

scholarly journals THE GROWTH CURVE OF THE LANSING STRAIN OF POLIOMYELITIS VIRUS IN THE CENTRAL NERVOUS SYSTEM OF THE MOUSE

1952 ◽  
Vol 95 (1) ◽  
pp. 1-7 ◽  
Author(s):  
John D. Ainslie
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Growth Curve ◽  
Clinical Signs ◽  
Virus Suspension ◽  
Poliomyelitis Virus ◽  
The Central Nervous System ◽  
Infectivity Titer ◽  
The Brain

After intracerebral inoculation of mice with a 10 per cent suspension (approximately 2000 LD50) of the Lansing strain of poliomyelitis virus, the infectivity titer in the brain decreased for approximately 6 hours. It then rose rapidly for 12 to 18 hours to reach titers of over 10–4. The rise in titer in the spinal cord closely paralleled that in the brain for 18 hours, after which the titer surpassed that in the brain by as much as one log. The infectivity titers in the central nervous system of unparalyzed mice remained between 10–3.5 and 10–4.2 for at least 7 days. With the onset of paralysis it was found that the titer was consistently and significantly higher in the spinal cords of paralyzed mice than in their brains or in the brains or cords of unparalyzed mice. After inoculation of 1 per cent virus suspension the increase in titer occurred about 9 hours later than after the inoculation of 10 per cent virus suspension, and the onset of clinical signs of illness was also delayed. Once the titers began to rise, the rate was the same after the inoculation of either concentration of virus, and the maximal levels reached were the same. With both concentrations of virus, maximal infectivity titers in non-paralyzed mice were reached about 9 hours before the onset of signs of poliomyelitis. The significance of these findings is discussed.

scholarly journals FATE OF NASALLY INSTILLED POLIOMYELITIS VIRUS IN NORMAL AND CONVALESCENT MONKEYS WITH SPECIAL REFERENCE TO THE PROBLEM OF HOST TO HOST TRANSMISSION

1938 ◽  
Vol 68 (1) ◽  
pp. 39-62 ◽  
Author(s):  
Albert B. Sabin ◽  
Peter K. Olitsky
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nasal Mucosa ◽  
Rhesus Monkeys ◽  
Olfactory Bulbs ◽  
Poliomyelitis Virus ◽  
The Central Nervous System ◽  
First Time ◽  
The Brain ◽  
Intranasal Instillation

With a method of intranasal instillation of poliomyelitis virus that brings about infection of all M. rhesus monkeys subjected to it, a study was undertaken of the fate of nasally instilled virus in normal and convalescent, immune animals. Control experiments revealed that nasal mucosa of normal monkeys contained no observable antiviral factors and that when five or ten minimal cerebral infective doses were added to the mucosa, virus could be detected by the employed procedure. In the olfactory bulbs even a single infective dose could be recovered, since suspensions of both bulbs could be transferred to the brain of a monkey without any loss of material. After nasal instillation of virus in normal monkeys, it disappeared quickly (4 hours or less) and could be recovered neither from the excised nasal mucosa nor from the olfactory bulbs during the first 48 hours. At 72 hours, just before or coincident with the first rise of temperature, virus was found in very small amounts in the nasal mucosa and for the first time also in the olfactory bulbs. At 96 hours, at least 3 days before the appearance of nervous signs, and later, while virus continued to be present in considerable amounts in the olfactory bulbs (and presumably elsewhere in the central nervous system), none was detected in the nasal mucosa. In convalescent, immune animals receiving the same strain of virus intranasally which caused the original infection, none could be recovered from the nasal mucosa or central nervous system at 4 hours, 1, 2, 3, 4, 5, and 7 days. The bearing of these observations on the problem of host to host transmission of poliomyelitis virus is discussed.

Glucuronyl 3-sulfate occurs exclusively on distal unmyelinated terminals of selected sensory neurons in the peripheral nervous system

1995 ◽  
Vol 53 ◽  
pp. 958-959
Author(s):  
S.S. Spicer ◽  
B.A. Schulte
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Peripheral Nervous System ◽  
Sensory Neurons ◽  
Sensory Nerves ◽  
Tissue Antigens ◽  
The Central Nervous System ◽  
The Brain ◽  
Leu 7

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.

Central Nerve System Impairment, AMA Guides, Sixth Edition: An Overview

2018 ◽  
Vol 23 (1) ◽  
pp. 10-13
Author(s):  
James B. Talmage ◽  
Jay Blaisdell
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Neurological Impairment ◽  
Sixth Edition ◽  
Central Nerve System ◽  
The Central Nervous System ◽  
The One ◽  
Nerve System ◽  
The Brain

Abstract Injuries that affect the central nervous system (CNS) can be catastrophic because they involve the brain or spinal cord, and determining the underlying clinical cause of impairment is essential in using the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), in part because the AMA Guides addresses neurological impairment in several chapters. Unlike the musculoskeletal chapters, Chapter 13, The Central and Peripheral Nervous System, does not use grades, grade modifiers, and a net adjustment formula; rather the chapter uses an approach that is similar to that in prior editions of the AMA Guides. The following steps can be used to perform a CNS rating: 1) evaluate all four major categories of cerebral impairment, and choose the one that is most severe; 2) rate the single most severe cerebral impairment of the four major categories; 3) rate all other impairments that are due to neurogenic problems; and 4) combine the rating of the single most severe category of cerebral impairment with the ratings of all other impairments. Because some neurological dysfunctions are rated elsewhere in the AMA Guides, Sixth Edition, the evaluator may consult Table 13-1 to verify the appropriate chapter to use.

RAS in the Central Nervous System: Potential Role in Neuropsychiatric Disorders

2018 ◽  
Vol 25 (28) ◽  
pp. 3333-3352 ◽  
Author(s):  
Natalia Pessoa Rocha ◽  
Ana Cristina Simoes e Silva ◽  
Thiago Ruiz Rodrigues Prestes ◽  
Victor Feracin ◽  
Caroline Amaral Machado ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Therapeutic Potential ◽  
Neuropsychiatric Disorders ◽  
Extensive Literature ◽  
Ang Ii ◽  
Mas Receptor ◽  
The Central Nervous System ◽  
The Brain

Background: The Renin-Angiotensin System (RAS) is a key regulator of cardiovascular and renal homeostasis, but also plays important roles in mediating physiological functions in the central nervous system (CNS). The effects of the RAS were classically described as mediated by angiotensin (Ang) II via angiotensin type 1 (AT1) receptors. However, another arm of the RAS formed by the angiotensin converting enzyme 2 (ACE2), Ang-(1-7) and the Mas receptor has been a matter of investigation due to its important physiological roles, usually counterbalancing the classical effects exerted by Ang II. Objective: We aim to provide an overview of effects elicited by the RAS, especially Ang-(1-7), in the brain. We also aim to discuss the therapeutic potential for neuropsychiatric disorders for the modulation of RAS. Method: We carried out an extensive literature search in PubMed central. Results: Within the brain, Ang-(1-7) contributes to the regulation of blood pressure by acting at regions that control cardiovascular functions. In contrast with Ang II, Ang-(1-7) improves baroreflex sensitivity and plays an inhibitory role in hypothalamic noradrenergic neurotransmission. Ang-(1-7) not only exerts effects related to blood pressure regulation, but also acts as a neuroprotective component of the RAS, for instance, by reducing cerebral infarct size, inflammation, oxidative stress and neuronal apoptosis. Conclusion: Pre-clinical evidence supports a relevant role for ACE2/Ang-(1-7)/Mas receptor axis in several neuropsychiatric conditions, including stress-related and mood disorders, cerebrovascular ischemic and hemorrhagic lesions and neurodegenerative diseases. However, very few data are available regarding the ACE2/Ang-(1-7)/Mas receptor axis in human CNS.

Ethanolamine: A Potential Promoiety with Additional Effects in the Brain

2020 ◽  
Vol 19 ◽  
Author(s):  
Asfree Gwanyanya ◽  
Christie Nicole Godsmark ◽  
Roisin Kelly-Laubscher
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Drug Design ◽  
Cell Signaling ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
The Central Nervous System ◽  
Bioactive Molecule ◽  
Positive Functions ◽  
The Brain

Abstract: Ethanolamine is a bioactive molecule found in several cells, including those in the central nervous system (CNS). In the brain, ethanolamine and ethanolamine-related molecules have emerged as prodrug moieties that can promote drug movement across the blood-brain barrier. This improvement in the ability to target drugs to the brain may also mean that in the process ethanolamine concentrations in the brain are increased enough for ethanolamine to exert its own neurological ac-tions. Ethanolamine and its associated products have various positive functions ranging from cell signaling to molecular storage, and alterations in their levels have been linked to neurodegenerative conditions such as Alzheimer’s disease. This mini-review focuses on the effects of ethanolamine in the CNS and highlights the possible implications of these effects for drug design.

scholarly journals Beyond Oncological Hyperthermia: Physically Drivable Magnetic Nanobubbles as Novel Multipurpose Theranostic Carriers in the Central Nervous System

Molecules ◽  
2020 ◽  
Vol 25 (9) ◽  
pp. 2104 ◽  
Author(s):  
Eleonora Ficiarà ◽  
Shoeb Anwar Ansari ◽  
Monica Argenziano ◽  
Luigi Cangemi ◽  
Chiara Monge ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Brain Tumors ◽  
Ad Hoc ◽  
Superparamagnetic Iron Oxide ◽  
Conventional Radiotherapy ◽  
The Central Nervous System ◽  
Magnetic Resonance Imaging Mri ◽  
The Brain

Magnetic Oxygen-Loaded Nanobubbles (MOLNBs), manufactured by adding Superparamagnetic Iron Oxide Nanoparticles (SPIONs) on the surface of polymeric nanobubbles, are investigated as theranostic carriers for delivering oxygen and chemotherapy to brain tumors. Physicochemical and cyto-toxicological properties and in vitro internalization by human brain microvascular endothelial cells as well as the motion of MOLNBs in a static magnetic field were investigated. MOLNBs are safe oxygen-loaded vectors able to overcome the brain membranes and drivable through the Central Nervous System (CNS) to deliver their cargoes to specific sites of interest. In addition, MOLNBs are monitorable either via Magnetic Resonance Imaging (MRI) or Ultrasound (US) sonography. MOLNBs can find application in targeting brain tumors since they can enhance conventional radiotherapy and deliver chemotherapy being driven by ad hoc tailored magnetic fields under MRI and/or US monitoring.

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