scholarly journals HISTOLOGICAL STUDIES ON HOG CHOLERA

1931 ◽  
Vol 53 (2) ◽  
pp. 277-287 ◽  
Author(s):  
Oskar Seifried

1. A more or less marked encephalomyelitis and meningitis was found in 33 out of 39 cases of virus hog cholera which had been infected either intramuscularly or by contact and killed between 6 and 49 days after infection. 2. This hog cholera encephalitis is characterized by a varying amount of vascular and perivascular infiltration with small lymphocytes, mononuclear elements, a few plasma cells, and occasionally a few eosinophilic leucocytes. The glia shows a proliferation surrounding infiltrated vessels or forming small nodules or more diffuse foci. Satellitism and in a few instances true neuronophagia have been observed. Both microglia and macroglia participate in this process. There is no essential increase of glia fibers. In nearly all parts of the central nervous system degenerating lesions of the nerve cells such as tigrolysis and degeneration of the nucleus, including a slight atrophy of endocellular neurofibers, are encountered. No demyelinization has been observed. Specific inclusion bodies in the nerve cells are absent. In addition, in a certain number of cases microscopic and macroscopic hemorrhages are present in the brain, spinal cord, and meninges. 3. These lesions in varying degrees have been found in swine infected with four different strains of hog cholera virus. Two were laboratory strains and two were obtained from fresh field outbreaks. 4. Histological changes in the central nervous system were found as early as 6 days after infection before the animal showed central nervous system symptoms. In two cases which were paralyzed no lesions in the central nervous system could be demonstrated. 5. The lesions in the central nervous system are considered to be the anatomical substratum for the various nervous symptoms commonly found in hog cholera.

2020 ◽  
Vol 74 ◽  
pp. 517-531
Author(s):  
Wioletta Kazana ◽  
Agnieszka Zabłocka

Brain-derived neurotrophic factor (BDNF) plays an important role in the proper functioning of the nervous system. It regulates the growth and survival of nerve cells, and is crucial in processes related to the memory, learning and synaptic plasticity. Abnormalities related to the distribution and secretion of BDNF protein accompany many diseases of the nervous system, in the course of which a significant decrease in BDNF level in the brain is observed. Impairments of BDNF transport may occur, for example, in the event of a single nucleotide polymorphism in the Bdnf (Val66Met) coding gene or due to the dysfunctions of the proteins involved in intracellular transport, such as huntingtin (HTT), huntingtin-associated protein 1 (HAP1), carboxypeptidase E (CPE) or sortilin 1 (SORT1). One of the therapeutic goals in the treatment of diseases of the central nervous system may be the regulation of expression and secretion of BDNF protein by nerve cells. Potential therapeutic strategies are based on direct injection of the protein into the specific region of the brain, the use of viral vectors expressing the Bdnf gene, transplantation of BDNF-producing cells, the use of substances of natural origin that stimulate the cells of the central nervous system for BDNF production, or the use of molecules activating the main receptor for BDNF – tyrosine receptor kinase B (TrkB). In addition, an appropriate lifestyle that promotes physical activity helps to increase BDNF level in the body. This paper summarizes the current knowledge about the biological role of BDNF protein and proteins involved in intracellular transport of this neurotrophin. Moreover, it presents contemporary research trends to develop therapeutic methods, leading to an increase in the level of BDNF protein in the brain.


1939 ◽  
Vol 85 (354) ◽  
pp. 119-125 ◽  
Author(s):  
R. E. Hemphill

On the subject of the correlation of neurological lesions with psycho-pathological phenomena, two eminent neuro-histologists, the Werthams, have recently written: “It must be pointed out that in proportion to the extraordinary complexity and differentiation of the finer functions mediated by the central nervous system, histological lesions are very gross. However we may conceive of the functional processes going on in the central nervous system—physiological, physico-chemical, metabolic, electrical, etc.—it should be obvious that only the grossest miscarriages and defects would become morphologically visible. Structural lesions are the effect of functional reactions that are not histologically demonstrable. Physico-chemical changes, metabolic processes, functional changes of blood-vessels, and similar biological phenomena that cannot be micro-histologically demonstrated, precede the anatomically visible lesions which occur only where the processes have attained a certain intensity. What we can demonstrate histologically in the nervous parenchyma is not by any means an adequate basis for the understanding of the quality, intensity or normality of nervous functions. In a patient who dies in the convulsions of tetanus, the anterior horn-cells may reveal nothing abnormal. Even the most minute and complete histological examination of the central nervous system in a case may fail to reveal any evidence of an existing profound disorder of brain function. There are cases of idiocy of the severest type in which no significant histological changes may be demonstrable in the brain.”


1970 ◽  
Vol 7 (5) ◽  
pp. 455-473
Author(s):  
W. Drommer ◽  
L.-Cl. Schulz ◽  
J. Pohlenz

Lesions are described in the central nervous system of 35 germ-free and 6 conventional piglets after experimental infection with different strains of Erysipelothrix insidiosa, type B. As controls 12 piglets were evaluated. The predominant findings were disturbance of permeability in the form of plasmadiapedesis and erythrodiapedesis, degeneration of neurons, and swelling of endothelial cells. Malactic foci were found in the brain stem, cerebrum and the grey matter of the cervical spinal cord of piglets belonging to three different groups. The lumens of vessels often contained free bacteria and activated monocytes with phagocytosed Erysipelas bacteria. The virulence of the strains of Erysipelas for gnotobiotic piglets was very different. Only Erysipelas strain T 28, type B, caused severe lesions in the central nervous system.


1878 ◽  
Vol 27 (185-189) ◽  
pp. 415-417

The brain of Mugil cephalus consists of three pairs and one unpaired tuberosity above, and two below. The most anterior pair are the olfactory lobes. From the anterior to posterior end they present four layers; first, olfactory nerve fibres with cell-like swellings upon them; second, coarsely granular neuroglia, with incipient glomeruli olfactorii, and large tripolar nerve cells; third, small usually unipolar cells each in its own space in the neuroglia; the whole collected into a rounded mass; fourth, nerve fibres proceeding from this mass to the second pair of tuberosities, the cerebral lobes, which consist of finely granular neuroglia, in which small cells are situated towards the circumference, and larger cells towards the centre, each of the latter contained in a lymph space.


Author(s):  
S.S. Spicer ◽  
B.A. Schulte

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.


2018 ◽  
Vol 23 (1) ◽  
pp. 10-13
Author(s):  
James B. Talmage ◽  
Jay Blaisdell

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.


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 ◽  
...  

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.


Author(s):  
Asfree Gwanyanya ◽  
Christie Nicole Godsmark ◽  
Roisin Kelly-Laubscher

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.


Molecules ◽  
2020 ◽  
Vol 25 (9) ◽  
pp. 2104 ◽  
Author(s):  
Eleonora Ficiarà ◽  
Shoeb Anwar Ansari ◽  
Monica Argenziano ◽  
Luigi Cangemi ◽  
Chiara Monge ◽  
...  

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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