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Immunomodulation of Cytokines and T Cells by Biologicals in Rheumatoid Arthritis
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Ravinder N. Maini, Marc Feldmann
Given these interesting data, the question that arises is whether anti-TNF therapy is a form of DMARD that could be effective in long-term control of RA. Since the duration of response to a single infusion of antibody is dose-dependent, lasting a median duration of 3, 6, and 8 weeks after a single infusion of 1, 3, and 10 mg/kg cA2 [69], long-term treatment would require repeated infusions of cA2. In an open study in which seven patients from the first “open label trial” received two or three further repeat cycles of cA2 after relapse of disease, with an observation period, in some cases, extending over a period of more than 1 year. After each sequential infusion, a reproducible clinical response of the same magnitude as the initial infusion was observed [46]. However, there appeared to be a trend toward a shortening of the response period, and in half the patients anti-human chimeric antibody directed against the murine idiotype developed. These results were encouraging in respect to the continuing dominance of TNFα over the cytokine network in RA but were inconclusive in respect to the possibility of continuing therapy. Further clinical trials were necessary to determine the efficacy of repeated therapy with a monoclonal antibody, not yet reported for any clinical indication, and to ascertain whether the immunogenicity of cA2 would be a limiting factor.
Central Nervous System Effects of Essential Oil Compounds
Published in K. Hüsnü Can Başer, Gerhard Buchbauer, Handbook of Essential Oils, 2020
Elaine Elisabetsky, Domingos S. Nunes
Temporal lobe epilepsy is one of the most common among the “difficult to treat” epilepsies, with almost a third of patients without adequate response to available treatments. In a rat intrahippocampal kainate experimental model of temporal lobe epilepsy, orally given thymoquinone decreased epileptic activity, reducing the increase in malondialdehyde (but not nitrite and nitrate) levels and SOD activity. Of note, 27 attenuated the hippocampal CA1 and CA3 neuronal loss and the signs of damage to the dentate nucleus, possibly suggestive of neuroprotective activity against the epileptic insult. The neuroprotection may be associated with the antioxidant and anti-inflammatory activities observed for this compound in other studies (Dariani et al., 2013).
The nervous system and the eye
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
James A.R. Nicoll, William Stewart, Fiona Roberts
Patients who sustain severe diffuse brain damage after cardiac arrest often die within a few days. The brain may appear normal macroscopically, but, if the patient has survived for more than 12 hours, microscopy shows widespread and severe neuronal necrosis with a distinctive pattern of selective vulnerability. Worst affected are the neocortex and hippocampus, with the greatest involvement of the CA1 sector. There is diffuse necrosis of the Purkinje cells of the cerebellum and loss of the sensory nuclei of the brainstem. In postmortem cases, brain damage is generally more severe in young children than adults. A similar pattern of damage may be seen in carbon monoxide intoxication, status epilepticus, and severe hypoglycaemia, although a slightly different pattern and distribution of pathology may be seen in the latter.
Neurotensin agonist PD 149163 modulates the neuroinflammation induced by bacterial endotoxin lipopolysaccharide in mice model
Published in Immunopharmacology and Immunotoxicology, 2022
Previous studies have reported that the LPS inhibited neurogenesis and accelerated the neuronal loss in the hippocampus, a key area of the brain responsible for cognitive and memory function and acting as a hotspot of neurogenesis [51]. The pyramidal cell loss in the hippocampus causes cognitive dysfunction and ultimately is modified into a neurodegenerative disorder. The hippocampus is vulnerable to inflammatory cytokines and oxidative stress. Some studies recently showed that the pro-inflammatory cytokines and ROS are responsible for neuronal death in the hippocampal area [60,61]. The CA1 and CA3 are two important sub-regions of the hippocampus made up of pyramidal cells; they act as a connecting link or neuronal circuit between the dentate gyrus and other brain areas, coordinating memory and cognitive function [26]. Therefore, in this study, we target the CA1 and CA3 regions to assess LPS-induced hippocampus deformities. We found that the LPS significantly altered the cytoarchitecture of the CA1 and CA3 region, as reported by others also [69]. CA1 and CA3 regions are marked with disorganization and pyramidal cell loss in the hippocampus, showing pale and darkened nuclei and shrinkage and vacuolization. This hippocampal atrophy might be corroborated with the reduced pyramidal cell layer thickness, pyramidal number and size of CA1 and CA3 regions. This evidence showed that the inflammatory cytokines, oxidative stress, and HPA axis activation were responsible for neuronal loss and thinning of pyramidal layers in the hippocampus.
Tramadol administration induced hippocampal cells apoptosis, astrogliosis, and microgliosis in juvenile and adult male mice, histological and immunohistochemical study
Published in Ultrastructural Pathology, 2020
Ola A. Hussein, Asmaa Fathi Abdel Mola, Amal Rateb
Interestingly, in the present work, the chronic tramadol administration induced morphological changes were detected in the three principal layers. Indeed, the vulnerability of CA3 versus CA1 pyramidal neurons differs according to different brain insults. Takuma, Nagai68 found that chronic restraint stress and ovariectomy can induce neuronal loss in hippocampal CA3 without neuronal loss in CA1 field and DG. Moreover, Medvedev, Ji69found different neuronal vulnerabilities according to the type of insult, as CA1 neurons may degenerate preferentially after global brain ischemia while CA3 can degenerate after limbic seizures. A possible important difference was also added as a rapid synaptic entry of Ca2+ and Zn2+ might more be involved in CA3, while the delayed and long-lasting accumulation of Zn2+ within mitochondria could contribute more in CA1.
C-Fos mapping and EEG characteristics of multiple mice brain regions in pentylenetetrazol-induced seizure mice model
Published in Neurological Research, 2019
Huajun Yang, Wei Shan, Fei Zhu, Tingting Yu, Jingjing Fan, Anchen Guo, Fei Li, Xiaofeng Yang, Qun Wang
Another phenomenon we found through EEG monitoring was that different brain regions showed different degrees of activation in response to seizure induction. The results showed that the hippocampal DG exhibited the most robust activation, CA3 also exhibited significant EEG response to seizure activity, and activation of hippocampal CA1, mPFC, the amygdala and the striatum was relatively moderate on EEG (Figure 2(b) and Table 2). These findings suggested that different brain regions have their own electrophysiological profiles in PTZ-induced seizures, which might reflect their respective roles in the occurrence and development of seizures. In PTZ-induced seizure model, it was reported that the hippocampal area was more likely involved in high-stage seizures such as generalized clonic or tonic-clonic seizures [2,14]. DG is the first hippocampal substructure to be activated in the local excitatory circuit in the hippocampus, which plays a key gating role in hippocampal excitation during seizures [17]. Additionally, the hippocampus has a relative low epileptogenic threshold; DG and CA3 have even lower threshold than other hippocampal subfields [18,19]. This might explain the robust EEG response in DG and CA3 compared with other brain areas. The degree of EEG activity in different brain regions might be associated with their involvement in seizures of certain types or severities and their excitability in response to epileptogenic stimuli.