scholarly journals Acute Nicotinamide Deficiency in the Pig Induced by 6-aminonicotinamide

1980 ◽  
Vol 17 (6) ◽  
pp. 748-758 ◽  
Author(s):  
B. M. O'Sullivan ◽  
W. F. Blakemore

Pigs given intraperitoneal injections of 6-aminonicotinamide developed a syndrome similar to a natural disease found in Queensland. Focal lesions, involving mainly destruction of glial cells, developed in the intermediate grey matter of the cervical and lumbar enlargement of the spinal cord. There was widespread vacuolation of spinal cord white matter. The glial cell loss was repaired. We suggest that natural acute nicotinamide deficiency can occur if a threshold dose of an antimetabolite of nicotinamide is absorbed over a short period of time.

2008 ◽  
Vol 15 (2) ◽  
pp. 180-188 ◽  
Author(s):  
CP Gilmore ◽  
JJG Geurts ◽  
N Evangelou ◽  
JCJ Bot ◽  
RA van Schijndel ◽  
...  

Background Post-mortem studies demonstrate extensive grey matter demyelination in MS, both in the brain and in the spinal cord. However the clinical significance of these plaques is unclear, largely because they are grossly underestimated by MR imaging at conventional field strengths. Indeed post-mortem MR studies suggest the great majority of lesions in the cerebral cortex go undetected, even when performed at high field. Similar studies have not been performed using post-mortem spinal cord material. Aim To assess the sensitivity of high field post-mortem MRI for detecting grey matter lesions in the spinal cord in MS. Methods Autopsy material was obtained from 11 MS cases and 2 controls. Proton Density-weighted images of this formalin-fixed material were acquired at 4.7Tesla before the tissue was sectioned and stained for Myelin Basic Protein. Both the tissue sections and the MR images were scored for grey matter and white matter plaques, with the readers of the MR images being blinded to the histopathology results. Results Our results indicate that post-mortem imaging at 4.7Tesla is highly sensitive for cord lesions, detecting 87% of white matter lesions and 73% of grey matter lesions. The MR changes were highly specific for demyelination, with all lesions scored on MRI corresponding to areas of demyelination. Conclusion Our work suggests that spinal cord grey matter lesions may be detected on MRI more readily than GM lesions in the brain, making the cord a promising site to study the functional consequences of grey matter demyelination in MS.


Author(s):  
Justin Yu ◽  
Neda Manouchehri ◽  
Shun Yamamoto ◽  
Brian K. Kwon ◽  
Thomas R. Oxland

2001 ◽  
Vol 168 (2) ◽  
pp. 213-224 ◽  
Author(s):  
Patricia Warden ◽  
Norman I. Bamber ◽  
Huaying Li ◽  
Andrew Esposito ◽  
Kaashif A. Ahmad ◽  
...  

2008 ◽  
Vol 56 (1) ◽  
pp. 117-123 ◽  
Author(s):  
Tolga Guvenc ◽  
Murat Yarim ◽  
Mustafa Gulbahar ◽  
Yonca Kabak

The cerebella of 12 dogs infected with canine distemper virus (CDV) and those of three normal dogs were examined. The avidin-biotin-peroxidase complex technique was used to detect αB-crystallin (αB-c) immunoreactivity and immunolocalisation of the CDV antigen. CDV antigens, immunopositive astrocytes, oligodendrocytes and granular neurons were seen in both the white and grey matter of the infected dogs. In the controls, αB-c immunopositive glial cells were seen in the white matter and around the Purkinje cells. In dogs with distemper, αB-c immunoreactivity was not observed in some of the glial cells around the Purkinje cells. A significant negative correlation of P < 0.01 level was found between areas of severe demyelination and the number of αB-c immunopositive cells in dogs infected with CDV. Such correlation was not observed between mild and moderate demyelinating areas and αB-c immunostaining. The αB-crystallin/total number of cells ratio was found to be significant in severely affected demyelinating areas (P < 0.05). These data indicate that there was a relationship between the degrees of CDV associated with demyelination and the level of αB-c expression in the glial cells.


1965 ◽  
Vol 2 (4) ◽  
pp. 360-379 ◽  
Author(s):  
Roy C. Anderson

The central nervous systems of five fawns (Odocoileus virginianus borealis), infected experimentally with Pneumostrongylus tenuis, were studied histologically 10, 20, 25, 30, and 40 days after infection. In the 10–30 day fawns young developing worms were found in dorsal horns of the grey matter of all regions of the spinal cord. A few worms were found in white matter and in the medulla oblongata. In the fawn autopsied 40 days after infection all but one of about 25 worms found were in the subdural space. Worms in the grey matter usually lay in cell-free tunnels surrounded by compressed neural tissue. There was little reaction of, or cellular infiltration in, surrounding tissue. Malacia was absent in all parts of grey matter. The central canal was normal and the brain, other than the medulla oblongata, was not involved. In the white matter, scattered single myelin sheath degeneration as well as degeneration and disappearance of axis cylinders were common. Occasionally there were tiny malacic areas in white matter, especially near worms. Infiltrations of eosinophils, lymphocytes, and plasma cells were commonly observed in and on the dura mater, the epineurium, ganglion capsules, and other tissues of the epidural space. The relative dearth of histopathologic findings helps to explain the rarity and slightness of neurologic signs in infected fawns and is indicative perhaps of a long and well established host-parasite relationship. This is in contrast to the situation in moose (Alces a. americana) where severe traumatic damage to the spinal cord by P. tenuis is associated with ataxia and paralysis.


2015 ◽  
Vol 6 (1) ◽  
pp. 3-6 ◽  
Author(s):  
Brian E. Cairns ◽  
Lars Arendt-Nielsen ◽  
Paola Sacerdote

AbstractBackgroundIt is unknown why an acute pain condition under various circumstances can transition into a chronic pain condition.There has been a shift towards neuroinflammation and hence glial cell activations specifically in the dorsal root ganglion and spinal cord as a mechanism possibly driving the transition to chronic pain. This has led to a focus on non-neuronal cells in the peripheral and central nervous system. Besides infiltrating macrophages, Schwann cells and satellite glial cells release cytokines and therefore important mechanisms in the maintenance of pain. Activated Schwann cells, satellite glial cells, microglia, and astrocytes may contribute to pain sensitivity by releasing cytokines leading to altered neuronal function in the direction of sensitisation.Aims of this perspective paper1) Highlight the complex but important recent achievement in the area of neuroinflammation and pain at spinal cord level and in the dorsal root ganglion.2) Encourage further research which hopefully may provide better understanding of new key elements driving the transition from acute to chronic pain.Recent results in the area of neuroinflammation and painFollowing a sciatic nerve injury, local macrophages, and Schwann cells trigger an immune response immediately followed by recruitment of blood-derived immune cells. Schwann cells, active resident, and infiltrating macrophages release proinflammatory cytokines. Proinflammatory cytokines contribute to axonal damage and also stimulate spontaneous nociceptor activity. This results in activation of satellite glial cells leading to an immune response in the dorsal root ganglia driven by macrophages, lymphocytes and satellite cells. The anterograde signalling progresses centrally to activate spinal microglia with possible up regulation of glial-derived proinflammatory/pronociceptive mediators.An important aspect is extrasegmental spreading sensitisation where bilateral elevations in TNF-α, IL-6, and IL-10 are found in dorsal root ganglion in neuropathic models. Similarly in inflammatory pain models, bilateral up regulation occurs for TNF-α, IL-1 β, and p38 MAPK. Bilateral alterations in cytokine levels in the DRG and spinal cord may underlie the spread of pain to the uninjured side.An important aspect is how the opioids may interact with immune cells as opioid receptors are expressed by peripheral immune cells and thus can induce immune signaling changes. Furthermore, opioids may stimulate microglia cells to produce proinflammatory cytokines such as IL-1.ConclusionsThe present perspective paper indicates that neuroinflammation and the associated release of pro-inflammatory cytokines in dorsal root ganglion and at the spinal cord contribute to the transition from acute to chronic pain. Neuroinflammatory changes have not only been identified in the spinal cord and brainstem, but more recently, in the sensory ganglia and in the nerves as well. The glial cell activation may be responsible for contralateral spreading and possible widespread sensitisation.ImplicationsCommunication between glia and neurons is proposed to be a critical component of neuroinflammatory changes that may lead to chronic pain. Sensory ganglia neurons are surrounded by satellite glial cells but how communication between the cells contributes to altered pain sensitivity is still unknown. Better understanding may lead to new possibilities for (1) preventing development of chronic pain and (2) better pain management.


2021 ◽  
Author(s):  
Ryan J Cali ◽  
Holly J Freeman ◽  
Benjamin Billot ◽  
Megan E Barra ◽  
David Fischer ◽  
...  

Pathophysiological mechanisms of neurological disorders in patients with coronavirus disease 2019 (COVID-19) are poorly understood, partly because of a lack of high-resolution neuroimaging data. We applied SynthSR, a convolutional neural network that synthesizes high-resolution isotropic research-quality data from thick-slice clinical MRI data, to a cohort of 11 patients with severe COVID-19. SynthSR successfully synthesized T1-weighted MPRAGE data at 1 mm spatial resolution for all 11 patients, each of whom had at least one brain lesion. Correlations between volumetric measures derived from synthesized and acquired MPRAGE data were strong for the cortical grey matter, subcortical grey matter, brainstem, hippocampus, and hemispheric white matter (r=0.84 to 0.96, p≤0.001), but absent for the cerebellar white matter and corpus callosum (r=0.04 to 0.17, p>0.61). SynthSR creates an opportunity to quantitatively study clinical MRI scans and elucidate the pathophysiology of neurological disorders in patients with COVID-19, including those with focal lesions.


2015 ◽  
Vol 22 (7) ◽  
pp. 910-920 ◽  
Author(s):  
Hugh Kearney ◽  
Katherine A Miszkiel ◽  
Marios C Yiannakas ◽  
Daniel R Altmann ◽  
Olga Ciccarelli ◽  
...  

Background: The in vivo relationship of spinal cord lesion features with clinical course and function in multiple sclerosis (MS) is poorly defined. Objective: The objective of this paper is to investigate the associations of spinal cord lesion features on MRI with MS subgroup and disability. Methods: We recruited 120 people: 25 clinically isolated syndrome, 35 relapsing–remitting (RR), 30 secondary progressive (SP), and 30 primary progressive (PP) MS. Disability was measured using the Expanded Disability Status Scale. We performed 3T axial cervical cord MRI, using 3D-fast-field-echo and phase-sensitive-inversion-recovery sequences. Both focal lesions and diffuse abnormalities were recorded. Focal lesions were classified according to the number of white matter (WM) columns involved and whether they extended to grey matter (GM). Results: The proportion of patients with focal lesions involving at least two WM columns and extending to GM was higher in SPMS than in RRMS ( p = 0.03) and PPMS ( p = 0.015). Diffuse abnormalities were more common in both PPMS and SPMS, compared with RRMS (OR 6.1 ( p = 0.002) and 5.7 ( p = 0.003), respectively). The number of lesions per patient involving both the lateral column and extending to GM was independently associated with disability ( p < 0.001). Conclusions: More extensive focal cord lesions, extension of lesions to GM, and diffuse abnormalities are associated with progressive MS and disability.


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