scholarly journals Bedaquiline has potential for targeting tuberculosis reservoirs in the central nervous system

RSC Advances ◽  
2018 ◽  
Vol 8 (22) ◽  
pp. 11902-11907 ◽  
Author(s):  
Annapurna Pamreddy ◽  
Sooraj Baijnath ◽  
Tricia Naicker ◽  
Sphamandla Ntshangase ◽  
Sipho Mdanda ◽  
...  

Bedaquiline (BDQ) was administered to healthy Sprague-Dawley rats in order to determine its localisation in the brain using mass spectrometry imaging (MSI). This study shows that BDQ has the potential for targeting TB reservoirs in the CNS.

Author(s):  
Ariel Y. Deutch ◽  
Robert H. Roth

Chapter 2 describes the neurochemical organization of the brain. It summarizes the diverse types of molecules that neurons in the brain use as neurotransmitters and neurotrophic factors, and how these molecules are synthesized and metabolized. The chapter also presents the array of receptor proteins through which these molecules regulate target neuron functioning and the reuptake proteins that generally terminate the neurotransmitter signal. Today a large majority of all drugs used to treat psychiatric disorders, as well as most drugs of abuse, still have as their initial targets proteins involved directly in neurotransmitter function.


Author(s):  
Michael J. Aminoff

In 1811, Bell had printed privately a monograph titled Idea of a New Anatomy of the Brain. In it, Bell correctly showed that the anterior but not the posterior roots had motor functions. François Magendie subsequently showed that the anterior roots were motor, and the posterior roots were sensory. This led to a dispute about priority during which Bell republished some of his early work with textual alterations to support his claims. Bell was involved in a similar dispute with Herbert Mayo concerning the separate functions of the fifth (sensory) and seventh (motor) cranial nerves, and Mayo today is a forgotten man. In both instances, Bell deserves credit for the concepts and initial experimental approach, and Magendie and Mayo deserve credit for obtaining and correctly interpreting the definitive experimental findings.


Metallomics ◽  
2014 ◽  
Vol 6 (3) ◽  
pp. 455-464 ◽  
Author(s):  
Ivan Lozić ◽  
Carole A. Bartlett ◽  
Jeremy A. Shaw ◽  
K. Swaminathan Iyer ◽  
Sarah A. Dunlop ◽  
...  

Nanoscale secondary ion mass spectrometry demonstrates that subsets of Ca microdomains rapidly decrease after central nervous system injury.


1988 ◽  
Vol 254 (3) ◽  
pp. E384-E388
Author(s):  
R. H. Safarik ◽  
R. M. Joy ◽  
D. L. Curry

This study reports that insulin is secreted in an episodic manner in rats and that the characteristics of its release can be modified by the central nervous system (CNS) and state of satiety. The pancreata of male Sprague-Dawley rats were perfused using the in situ brain-pancreas technique under urethan anesthesia. Episodic insulin release under non-fasted conditions was not altered by the presence or absence of CNS innervation to the pancreas. Under these conditions the interpeak period was 5.9 and 6 min, respectively, and cycle length was 3.7 and 4 min. However, perfusions that were performed following an overnight fast demonstrated that the CNS is capable of modulating episodic insulin release. After fasting, when comparing CNS-ablated with -intact preparations, the period was shortened from 5.2 to 4.1 min (P less than 0.05), and the number of episodes per 90-min perfusion increased from 16.0 to 19.0 (P less than 0.05) when the pancreas was innervated by the CNS. Additionally, the effect of fasting on denervated pancreata resulted in a shortening of the cycle length, which was prevented when the CNS was functional. These results demonstrate that episodic insulin release can be modified by metabolic conditions and are subject to mediation by the CNS.


Author(s):  
Michael R. Keating

Infections of the central nervous system include meninigitis (acute and chronic), encephalitis, myelitis, abscesses, and cerebrospinal fluid shunt infections. Meningitis is diagnosed by the presence of white blood cells in the cerebrospinal fluid. Encephalitis is inflammation of the brain caused by infection. Myelitis is infection or inflammation of the spinal cord. The diagnosis and treatment of various types of central nervous system infections are reviewed.


1983 ◽  
Vol 244 (6) ◽  
pp. H807-H813 ◽  
Author(s):  
T. Okuno ◽  
S. R. Winternitz ◽  
M. D. Lindheimer ◽  
S. Oparil

To determine whether impaired arginine vasopressin (AVP) release occurs when DOCA-NaCl hypertension is prevented following chemical sympathectomy with 6-hydroxydopamine (6-OHDA), male Sprague-Dawley rats treated with intraventricular injections of 6-OHDA (250 micrograms X 2) or Merlis solution received deoxycorticosterone acetate (DOCA) implants (100 mg/kg) and drank 0.5% saline. Systolic blood pressure in the 6-OHDA-treated DOCA/NaCl group (139 +/- 4 mmHg) was lower (P less than 0.001) than in the Merlis-DOCA/NaCl group (183 +/- 7 mmHg). 6-OHDA treatment produced widespread catecholamine depletion throughout the central nervous system, including the supraoptic and paraventricular nuclei, the cells of which are known to produce AVP, but hypothalamic, pituitary, and plasma AVP levels were similar in both experimental groups, the latter values averaging 1.5–2 times those of controls. Both groups of rats suppressed AVP secretion appropriately when water loaded. Such suppression, however, had no effect on blood pressure in the hypertensive animals and, furthermore, administration of the AVP antagonist d(CH2)5Tyr(Me)AVP produced small decrements in mean blood pressure of both groups that were not significantly different from responses seen in control normotensive rats. These data demonstrate that 6-OHDA does not prevent DOCA-NaCl hypertension by decreasing AVP levels and suggest that AVP is not necessary for the maintenance of hypertension in this model.


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.


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