Open Access Pub publishes peer-reviewed, free-to-read open-access articles. Showing
articles matching Nervous System — open any to read the full text,
or download the PDF or XML.
Mar 2022 DOI 10.14302/issn.2471-7061.jcrc-22-4139
Wu JianqingCorresponding author
Healthier World (Independent researcher for cause), P. O. Box 689, Beltsville, MD 20704. USA
We examined special roles of the Central Nervous System (CNS) in an attempt to resolve the puzzle that chronic diseases cannot be cured in medicine. By exploring a skill-learning model, we found that the CNS is able to remember certain information reflecting biochemical and cellular (B&C) processes in the body. From the skill-using ability, we found that the CNS is able to control basic B&C processes that drive and power the skill. From the ability to adjust forces and moving direction of body parts, we infer that the CNS is able to adjust B&C processes that control physical acts. From this controlling capability, we inferred that the CNS must also store certain information on the baseline B&C processes, is able to up-regulate or down-regulate the B&C processes, and make comparisons in performing its regulatory functions. We found that chronic diseases are the results of deviated baseline B&C processes, the CNS plays a role in maintaining deviated baseline B&C processes, and protects the body state of a fully developed disease. The three CNS roles can explain that cancer progresses with increasing malignancy, cancer quickly returns after a surgery, cancer cells repopulate after chemotherapy and radiotherapy, cancer patients develop drug resistance inevitably, immune cells rebound after suppression, etc. We further showed that long-term exercises generally can correct part of the departures in B&C processes and thus help to reverse chronic diseases. Finally, we propose strategies for resetting the CNS’ state memory as an essential condition for curing chronic diseases and cancer.
Feb 2020 DOI 10.14302/issn.2641-5518.jcci-20-3166
Bruno Bidin Brooks JosephCorresponding author
Department of Structure and Function, UNIMES- Universidade Metropolitana de Santos, São Paulo, Brazil
This case documents a pseudotumoral CNS lesion in Behcet's disease with sustained response to infliximab therapy. Clinical evolution, neuroimaging changes, and rationale for TNF‑alpha inhibition are detailed. The report supports considering biologic therapy for refractory neuro‑Behcet manifestations under specialist guidance.
Jun 2017 DOI 10.14302/issn.2470-5020.jnrt-17-1529
Drobnik JaroslawCorresponding author
Gerontology Unit, Public Health Department, Health Sciences Faculty, Wroclaw Medical University,
Epidemiological data concerning malignant neoplasms of meninges and central nervous system parts other than brain in Poland are reported to many medical databases run by various institutions and are incongruent with each other which makes their practical interpretation highly difficult. Data on registered cases of malignant neoplasms of meninges (C70-C70.9 ICD-10) and of spinal cord, cranial nerves and parts of central nervous system other than brain (C72-C72.9 ICD-10) in the years 2006-2012, made available by public healthcare insurance provider Narodowy Fundusz Zdrowia in Lower Silesia region of Poland (NFZ) and data on new cases from Polish national neoplasms registry Krajowy Rejestr Nowotworow (KRN), were analyzed. The study revealed that those neoplasms are rare in Lower Silesia region of Poland population, number of new cases dropped in the analyzed period, but the NFZ/KRN cases ratio increased significantly especially in case of malignant neoplasms of central nervous system parts other than brain or meninges, which suggests big, and increasing with time, amount of medical procedures needed by those patients. It points at the need of respective adjustment of the level of public financing of treatment of malignant neoplasms of meninges and other central nervous system parts than brain. The study results indicate also that epidemiological reporting system in Poland shall be improved as there is growing number of Polish physicians who report mainly unspecific broad ICD-10 categories and there are year-to-year alternations of reported numbers of cases that do not have any explanation other than formal shifting in reported ICD-10 categories.
Jun 2014 DOI 10.14302/issn.2372-6601.jhor-14-378
Kulma-Kreft MonikaCorresponding author
Department of Radiotherapy and Medical Oncology, Gdynia Cancer Center, Gdynia
Progressive multifocal leukoencephalopathy (PML) is a rare complication associated, inter alia, with rituximab-based lymphoma treatment. PML diagnosis is made easier with the criteria recently published by the American Academy of Neurology. Unambiguous diagnosis of PML can be achieved by demonstration of the histopathological triad comprising:(1) demyelination, (2) bizarre astrocytes and (3) enlarged oligodendroglial nuclei together with detection of viral particles by electron microscopy. However, symptoms of PML may be similar to those observed during lymphoma progression into the central nervous system (CNS). Here we report the case of a patient with diffuse large B-cell lymphoma (DLBCL) treated with R-CHOP who developed clinical signs indicating PML. Intravital diagnostic methods failed to yield an unequivocal diagnosis of PML or lymphoma progression in the CNS. However, a post-mortem examination of brain biopsy specimens performed by electron microscopy demonstrated lesions typical for PML and the presence of viral particles. In addition, immunohistochemical assays identified a massive infiltration of lymphoma cells. The case thus suggests either the extremely rare coexistence of two complications: lymphoma CNS infiltration and PML or induction structural CNS lesions by lymphoma infiltration indistinguishable from PML. The presented findings thus highlight the need for a further review of the current diagnostic criteria for PML.
Jun 2024
Rahbani AbdallahCorresponding author
Multiple Sclerosis has traditionally been considered an inflammatory and autoimmune disease of the central nervous system. However, peripheral cranial nerve involvement has been described previously in eight cases, raising the hypothesis of a disease spectrum between central and peripheral nervous system. We hereby present a case of a 12 years old girl diagnosed with Multiple Sclerosis who presents with complete unilateral third cranial nerve palsy. Complete clinical, laboratory and radiological work-up was consistent with demyelinating disease. We conclude that demyelination in Multiple Sclerosis can affect in some cases both the central and peripheral nervous system.
Mar 2024 DOI 10.14302/issn.2689-4602.jes-24-4982
O. Henderson JeffreyCorresponding author
Mammalian Rbm45 is predominately expressed in neuronal tissue and is integral in brain development and neuronal differentiation under physiological conditions. Dysregulation of Rbm45 has been strongly associated with neurodegenerative disorders in humans and can drive hepatocellular carcinoma through reprogramming lipid metabolism. Intriguingly, Rbm45 is an ancient protein, evolutionarily conserved throughout metazoans, including in sponges which lack a nervous system. Curiously, the evolution of Rbm45 gene structure and protein domain conservation across kingdom Animalia is largely unknown. We performed phylogenetic analysis of Rbm45 nucleotide and amino acid sequences from 36 species representing 9 phyla: Porifera, Cnidaria, Priapulida, Mollusca, Brachiopoda, Arthropoda, Echinodermata, Hemichordata, and Chordata. While the tree from Rbm45 nucleotide sequence data resulted in clades Protostomia and Deuterostomia showing paraphyly, the phylogeny derived from Rbm45 amino acid sequence largely recapitulated known monophyletic relationships among metazoans. Human RBM45 protein structure includes three RNA-binding domains (RBD), a homo-oligomerization association (HOA) domain, a nuclear localization sequence (NLS), and a nuclear export sequence (NES). Multiple sequence alignment across the same 36 taxa used for phylogenetic analysis revealed conservation of all three RBDs, the HOA, and NLS; in contrast the NES was only detected in clade Craniata and not in clades Ambulacraria and Protostomia. Rbm45 gene structure analysis revealed increasing gene complexity concomitant with increasing evolutionary complexity. Rbm45 from non-bilaterian taxa had from 2 to 4 large exons, while bilaterian taxa had between 6 to17 small exons. These findings demonstrate that Rbm45 is an ancient, highly conserved gene among metazoans suggesting a function in a breadth of neural/sensory systems.
Dec 2023 DOI 10.14302/issn.2693-1176.ijgh-23-4854
Isea RaulCorresponding author
A potential treatment for Alzheimer's disease is vagus nerve therapy, which has been made possible by considerable advances in neuroscience. An essential component of the autonomic nervous system, the vagus nerve regulates memory, inflammation, and cognition. Researchers hope to delay the progression of Alzheimer's disease and improve cognitive function by implanting a vagus nerve stimulator (VNS). Alzheimer's patients have higher heart rate variability, according to an ECG study, which may be advantageous. To completely grasp its mechanics and long-term effectiveness, more research is necessary.
Jun 2022 DOI 10.14302/issn.2470-5020.jnrt-22-4217
O. Henderson JeffreyCorresponding author
Department of Science and Mathematics, Judson University, Elgin, IL 60123, USA
Tay-Sachs disease (TSD) is a rare neurodegenerative disorder caused by mutations in the HEXA gene, which encodes the ɑ subunit of the enzyme β-hexosaminidase A. Lacking this key enzyme in GM2 ganglioside catabolism, individuals who are homozygous for HEXA mutations suffer from abnormal accumulation of GM2 ganglioside in brain and nerve cells, ultimately resulting in the progressive deterioration of the central nervous system. TSD is one of three disorders characterized by β-hexosaminidase deficiency; Sandhoff disease (SD) and the AB variant arise by mutations in the HEXB and GM2A genes respectively, which disrupt other points of GM2 ganglioside degradation. Characterized by developmental delay and stagnation, muscular weakness, coordination deficits, seizures, and eventual hearing and vision loss, these three disorders are clinically indistinguishable and occur in three forms defined by age of onset. While there is a much higher incidence of TSD in the Ashkenazi Jewish population, community carrier screening and counseling initiatives have reduced disease prevalence to about the equivalent of non-Jewish populations; however, such efforts have raised ethical concerns in the Jewish community that are increasingly relevant in light of scientific and medical advancements. Currently, treatments for TSD and its related disorders focus on symptom management, with gene therapies and the application of modified CRISPR-Cas-9 technology being explored.
Feb 2022 DOI 10.14302/issn.2470-5020.jnrt-22-4092
AGBA LéhlengCorresponding author
Neurology Department, Intercommunal Hospital of Poissy/Saint-Germain-En-Laye, Poissy – France
Acute disseminated encephalomyelitis (ADEM) is a monophasic, multifocal, demyelinating, autoimmune disease that affects the central nervous system (CNS). It usually occurs after a systemic infection, usually viral, including certain coronavirus infections. A 27-year-old girl presented with complaints of left interscapular pain, paresthesias and weakness in the ipsilateral upper limb. These symptoms followed paresthesias on the fingertips of her right hand the day before her admission. she was treated two weeks earlier for pneumonia with COVID-19. Her clinical pattern resulted in a moderate weakness of the left limbs associated with tactil and algic hypoesthesia in the lower left limb ascending until the C4 level in the left side. Magnetic resonance imaging (MRI) of the brain and spinal cord showed diffuse spontaneous hypersignals on fluid-attenuated inversion recovery (FLAIR) images at the cerebral level and on T2-weighted images at the spinal level. These imaging lesions coupled with the medical history of a recent COVID-19 infection led to the diagnosis of acute disseminated encephalomyelitis (ADEM) post covid-19. The clinical condition improved rapidly with intravenous (IV) corticosteroid therapy and IV immunoglobulin combined with physiotherapy. ADEM is a demyelinating autoimmune disease which is increasingly reported during this current corona virus pandemic.
Aug 2020 DOI 10.14302/issn.2694-1201.jsn-20-3523
Nasim Habibzadeh SeyedehCorresponding author
PhD student in Sport Science, School of Health and Life Sine, Department of Sport Science, Teesside University, United Kingdom
The brain requires certain fuels to function in high level. Literally, nutritional components can modulate the brain productivity. One of the right nutrition to enhance the brain power is dietary component of caffeine. Caffeine as a component of coffee, tea and chocolate is very popular. Although, depending on the dietary demands or conventional habits some people do not consume caffeine-containing substances (i.e. foods or beverage). Nonetheless, caffeine constituents maximize the brain potential via promoting the central nervous system (CNS) through blocking an inhibitory neurotransmitter (adenosine) and releasing some other specific neurotransmitters (noradrenaline, dopamine and serotonin) in brain. The chemistry of caffeine in a standard dose in fact can affect the brain intelligence.
Jul 2020 DOI 10.14302/issn.2576-6694.jbbs-20-3450
M. Mahmoud MagdyCorresponding author
Faculty of Science, Ain Shams University, Cairo Egypt.
Background Hyperphenylalaninemia (HPA) combined with neurological signs due to impaired catecholamine, dopamine and serotonin synthesis. Symptoms may appears in first week of life but most seen in age of 4 months. Atypical PKU disease caused mainly by deficiency in 6-pyruvoyltetrahydropterin synthase (PTPS) involved in synthesis of BH4. Clinical symptoms may include poor sucking, impaired tone, ataxia, and seizures. The purpose of this study was to analyze the genotype-phenotype relation among BH4 deficient patients because of PTPS mutations in different state of Egypt. Methods Suspected PKU patients loaded with phenylalanine/Kuvan, and the level of phe and phe/tyrosine ratio determined using tandem mass spectrometry by dried blood spots. Blood samples of 13 unrelated Egyptian patients were collected for total RNA extraction, amplification of PTPS gene by PCR followed with sequencing by Sanger method and finally mutations were recorded for genetic analysis. Results The mean value of phe in 13 patients decreased after loaded of phenylalanine from 482.5μmol/L to 270.63 μmol/L as well as phe/tyrosine ratio was decreased from 13.4 to 6.36 after 24hour of treatment with Kuvan. Sanger sequencing of PTPS gene of those patient showed 21 SNPs and Indels mutations. The most repeated mutation is a novel 23 base pair homozygous deletion in 12/13; c.200C>T in four patients, a novel c.86A>T in two patients and three different mutations located once in three different patients (novel c.22C>T; novel c.273G>A and 405T>C) among patients. On amino acid predicted sequences 4 different types of mutations on protein level were presented, 1 deletion mutation in seven amino acid and 3 different missense mutations in addition to 2 silent mutations among 13 patients. Conclusion Patients were the first case of clinical diagnosis as hyperphenylalaninemia (HPA) undergoing genetic diagnosis for PTPS deficiency in Egypt. The sever HPA patients with severe nervous system damage mainly accompanied with deletion mutations and should pay more attention to the BH4 deficiency. While mild HPA is associated with base substitution mutations with mainly transition mutations (7/9; 78%). Next-generation sequencing technique can increase the mutation detection rate when the hereditary diseases are highly suspected in clinic.
Nov 2019 DOI 10.14302/issn.2574-4526.jddd-19-3063
I Alvarez-Leite JacquelineCorresponding author
Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerias, Brazil.
Most of the patients with inflammatory bowel disease avoid pepper or spicy food, alleging that this condiment causes anal sensation of burning and accelerates intestinal movements. Capsaicin is the main bioactive component of peppers responsible for the pungent flavor that characterizes red peppers. Capsaicin has been related to several biological effects, including decreased body fat, antianti-inflammatory, anticarcinogenic, antioxidant activites and modulator of intestinal motility. These actions mostly are due to its role as an agonist of the transient receptor potential vanilloid 1 (TRPV1), expressed in the mesenteric nervous system and epithelial cells of the colon. Nonetheless, the anti-inflammatory action of capsaicin is also related to its role in activating the peroxisomal proliferator-activated receptor gamma (PPAR-γ). Topical capsaicin formulations are already used for pain management, but oral administration of capsaicin is rare. Here, we discuss the main actions of capsaicin that could interfere with the symptoms and severity of IBD. Although animal experiments suggest a beneficial effect of capsaicin on colitis, clinical studies exploring the potential analgesic and anti-inflammatory of capsaicin on Crohn or Ulcerative Colitis are scarce. We concluded that there is no evidence that capsaicin aggravates IBD symptoms or severity. On the opposite, experimental studies suggest that capsaicin could reduce intestinal inflammation by a mechanism that could involve not only the TRPV1 receptor but also PPAR γ. However, clinical studies are still scarce, and data regarding capsaicin concentrations, routes of administration, and long-term side-effects need to be better understood before its use.
Oct 2018 DOI 10.14302/issn.2577-2279.ijha-18-2407
Fu HuiCorresponding author
Shenzhen Institute of Wuhan University, Shenzhen, china.
Oligodendrocytes are specialized glial cell in central nervous system (CNS) responsible for the formation of myelin sheath around the axon. Oligodendrocyte proliferation and differentiation is regulated by Wnt signaling pathway, at various stages. However, different study groups have described controversial conclusions about the effect of Wnt on oligodendrocytes precursor cells (OPCs) development. Initially it has been proposed that Wnt pathway negatively regulates the OPCs proliferation and differentiation but recently some studies have described that Wnt promotes the differentiation of OPCs. After carefully reviewing the literature, we believe that Wnt play multiple roles in OPCs differentiation and its function is time (stage) and dose sensitive. Low to moderate activation of Wnt promotes OPC development, while too much or too low is inhibitory. Current evidences also suggested that in early developmental stages, Wnt inhibits the OPCs formation from neural progenitors and differentiation into immature oligodendrocytes. But in late stages Wnt plays promoting role in differentiation and maturation of oligodendrocytes. This review summarized the updated information regarding the critical role of Wnt signaling cascade in proliferation and differentiation of OPCs.
May 2017 DOI 10.14302/issn.2470-0436.jos-17-1453
Zhang JieCorresponding author
Department of Ophthalmology, Faculty of Medical and Health Sciences, University of Auckland, Private bag 92019, Auckland 1142, New Zealand.
Purpose: High intraocular pressure (IOP) is known to result in retinal ganglion cell (RGC) loss, both with chronically raised intraocular pressure (such as with glaucoma) and with acute raises in pressure (due to injury or acute angle closure). Because IOP is often raised during ocular surgery, the purpose of this study was to evaluate the effect of transient moderate IOP on retinal function, RGC survival and the expression of Connexin 43 (Cx43) and glial fibrillary acidic protein (GFAP), ubiquitously expressed central nervous system (CNS) proteins that are known to be elevated during the retinal inflammatory response to injury. Materials and Methods: Wistar rats were exposed to transient IOP at 40 mmHg for 5 or 30 minutes, and 60 mmHg for 5 minutes (via cannulation of the anterior chamber with a saline reservoir raised to a height corresponding to the desired IOP), mimicking potential IOP rises during surgery such as DSAEK and some laser procedures (LASIK and femtosecond laser cataract surgery). Separate groups of animals had IOP maintained at 10 mmHg for 5 or 30 minutes as cannulation controls, or 120 mmHg for 60 minutes as positive controls. Changes in the optic nerve and retina were assessed immunohistochemically for GFAP and Cx43 expression. Retinal function was assessed using electroretinography (ERG) recorded at baseline and 14 days after the IOP rise and compared with RGC counts. Results: Results showed that there was a differential GFAP labelling pattern observed in the anterior optic nerve in the 40 mmHg 30 minute and 60 mmHg 5 minute groups 4 hours after manipulation. Gap junction protein Cx43 was minimally up-regulated in the retina in the short-term. There was, however, minimal long-term effect on retinal function and no RGC loss. Conclusions: n conclusion, elevations of IOP that are short in duration such as those occurring during surgical procedures, do not cause significant changes long-term in retinal function or RGC survival. Key Messages: Cx43 and GFAP are known to be elevated during the retinal inflammatory response to injury. No previous study has explored the effect of moderate and relatively short increases in IOP on the initial inflammatory response. We observed a mild glial inflammatory response in the anterior optic nerve, but only a minimal up-regulation of Cx43. However, transient and moderate IOP rises did not induce long term disruption to RGC function or number as measured by electrophysiology and RGC counts, respectively. This is applicable to clinical practice, as it means the IOP elevations that occur during some surgical procedures are unlikely to be causing long term damage in retinal function or RGC survival.
Mar 2014 DOI 10.14302/issn.2326-0793.jpgr-13-333
C. Ghosh ManikCorresponding author
Department of Physiology, University of Tennessee Health Science Center, 894 Union Avenue, Memphis, TN, 38163.
Carbofuran is a broad spectrum pesticide used in agricultural fields and domestic places throughout the world. It is one of the deadly toxic carbamate pesticide that kills the pest by inhibiting the crucial enzyme of nervous system known as acetyl cholinesterase. In the present study, we report how carbofuran increases the different spectrum of cholesterols, including free cholesterol and esterified cholesterol in the fish hepatocytes. It is observed that induced-cholesterol can inhibit the enzymatic activity such as Ca++-ATPase, which is a critical protein for maintaining the calcium homoeostasis in the cellular microenvironment. Carbofuran integrates into human body through foods and drinks. As trace of carbofuran is identified in our daily food and drinks, we examined the homology of Ca++-ATPase between the fish and human, so our data can illuminate the effects of carbofuran on this crucial enzyme. While studying the homology with the help of bioinformatics, we recognized that there is around 70% homology in the protein sequence of Ca++-ATPase between fish Heteropneustesfossilisand human (Homo sapiens), which appears as sufficient to simulate our fish-model data in human. This study demonstrates that carbofuran affects our day-to-day life by inhibiting Ca++-ATPase through modulation of lipid synthesis, a critical regulatory system that controls overall homeostasis in our body.