Relevant bibliographies by topics / Immunological aspects of Neurocutaneous disorders

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Immunological aspects of Neurocutaneous disorders'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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Journal articles on the topic "Immunological aspects of Neurocutaneous disorders"

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Jentarra, Garilyn, Shannon L. Snyder, and Vinodh Narayanan. "Genetic Aspects of Neurocutaneous Disorders." Seminars in Pediatric Neurology 13, no. 1 (2006): 43–47. http://dx.doi.org/10.1016/j.spen.2006.01.010.

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Eeg-Olofsson, Orvar. "Virological and immunological aspects of seizure disorders." Brain and Development 25, no. 1 (2003): 9–13. http://dx.doi.org/10.1016/s0387-7604(02)00162-6.

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Nagata, Toshihiko, and Hisashi Yamada. "Psycho-neuro-immunological aspects of eating disorders." International Congress Series 1287 (April 2006): 279–84. http://dx.doi.org/10.1016/j.ics.2005.11.097.

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Kupka, R. W., M. H. J. Hillegers, W. A. Nolen, N. Breunis, and H. A. Drexhage. "Immunological aspects of bipolar disorder." Acta Neuropsychiatrica 12, no. 3 (2000): 86–90. http://dx.doi.org/10.1017/s092427080003547x.

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ABSTRACTIntroduction: Significant changes in immune function have been found in mood disorders. Controlled studies in bipolar disorder concerning cell-mediated immunity and thyroid autoimmunity are reviewed, and presented together with preliminary findings from our own ongoing study.Method: Using Medline and other sources, 14 controlled studies as well as some other relevant studies were found.Results: Bipolar disorder is associated with an acute phase response and activation of the cell-mediated immune system, and with an increased prevalence of antithyroid autoantibodies.Conclusion: Changes in immune function, in connection with neuroendocrine changes, may provide new hypotheses for the pathophysiology of mood disorders.
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Monticelli, Maria, Tiago Ferro, Jaak Jaeken, Vanessa dos Reis Ferreira, and Paula A. Videira. "Immunological aspects of congenital disorders of glycosylation (CDG): a review." Journal of Inherited Metabolic Disease 39, no. 6 (2016): 765–80. http://dx.doi.org/10.1007/s10545-016-9954-9.

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Altinoz, Meric A., and Bahri Ince. "Hemoglobins emerging roles in mental disorders. Metabolical, genetical and immunological aspects." International Journal of Developmental Neuroscience 61, no. 1 (2017): 73–85. http://dx.doi.org/10.1016/j.ijdevneu.2017.06.007.

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Nicolaisen, Else Marie, Lisbeth Lyng Hansen, Fritz Poulsen, Steven Glazer, and Ulla Hedner. "Immunological Aspects of Recombinant Factor Vila (rFVIIa) in Clinical Use." Thrombosis and Haemostasis 76, no. 02 (1996): 200–204. http://dx.doi.org/10.1055/s-0038-1650554.

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SummaryPatients, receiving rFVIIa for treatment of bleeding disorders, have been followed for specific antibody formation. No antibodies against FVII were demonstrated in 170 patients, with hemophilia, or with acquired inhibitors to clotting factors. Of 6 FVII-deficient patients, one overdosed patient developed antibodies to human FVII. There was no indication of de novo formation of antibodies to potential contaminating foreign protein, which could be correlated to the rFVIIa treatment. Except for the FVII-deficient population, which may represent a risk group, rFVIIa appears to be immunologically safe for use in patient groups with bleeding disorders, including hemophilia A and B patients.
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Di Stefano, Vincenzo, Filomena Barbone, Camilla Ferrante, et al. "Inflammatory polyradiculoneuropathies: Clinical and immunological aspects, current therapies, and future perspectives." European Journal of Inflammation 18 (January 2020): 205873922094234. http://dx.doi.org/10.1177/2058739220942340.

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Inflammatory polyradiculoneuropathies are heterogeneous disorders characterized by immune-mediated leukocyte infiltration of peripheral nerves and nerve roots leading to demyelination or axonal degeneration or both. Inflammatory polyradiculoneuropathies can be divided into acute and chronic: Guillain–Barré syndrome and chronic inflammatory demyelinating polyneuropathy and their variants. Despite major advances in immunology and molecular biology have been made in the last years, the pathogenesis of these disorders is not completely understood. This review summarizes the current literature of the clinical features and pathogenic mechanisms of inflammatory polyradiculoneuropathies and focuses on current therapies and new potential treatment for the future.
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Vasil’ev, Ivan M., A. V. Muranova, E. S. Smirnova, L. I. Bogdanets, and V. I. Sinopal’nikov. "Pathogenetic aspects of venous trophic ulcers and approaches to correction of immunological disorders." Clinical Medicine (Russian Journal) 94, no. 11 (2017): 820–26. http://dx.doi.org/10.18821/0023-2149-2016-94-11-820-826.

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The review deals with the problem of venous trophic ulcers. Current data on epidemiology and social significance of this condition are presented with special reference to pathogenetic aspects of its development, such as systemic immunity disorders associated with chronic venous insufficiency. The necessity and possibility of correction of some of them are discussed.
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Pinching, Anthony J. "Clinical and immunological aspects of the acquired immune deficiency syndrome and related disorders." Journal of Hospital Infection 6 (December 1985): 1–8. http://dx.doi.org/10.1016/s0195-6701(85)80002-5.

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Dissertations / Theses on the topic "Immunological aspects of Neurocutaneous disorders"

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Kong, Wai-kwan Wendy, and 江慧君. "The effects of immune activation in the pathogenesis of neurodevelopmental disorders : in vivo and in vitro animal studies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/197539.

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Schizophrenia and autism are psychiatric disorders with a presumed neurodevelopmental origin, characterised by clinical features and aetiologies that overlap at multiple levels. In addition to genetic susceptibility, epidemiological studies revealed an association between environmental factors and these disorders. Immune activation in response to infection at early gestation has been identified as one of the key risk factors. Little is known about the underlying mechanism during maternal immune activation (MIA), but extrinsic apoptotic dysregulation has been postulated to play a role in MIA infection. In particular, emerging studies suggest apoptosis without triggering whole cell demise, namely synaptic apoptosis, is a potential event that leads to the abnormal behaviours in the affected offspring. In this study, C57BL/6N mice model was employed to investigate the impacts of viral mimetic polyriboinosinic-polyribocytidylic acid (Poly I:C) exposure at gestation day 9 in the resultant male offspring in adulthood in vivo by different parameters, including magnetic resonance imaging (MRI), behavioural tasks that assess sensorimotor gating, exploratory and anxiety behaviours, and protein quantification in the apoptotic pathway. In parallel, the direct effect of Poly (I:C) treatment for 24 hours on extrinsic apoptotic proteins were determined in primary cortical neurons in vitro. It was hypothesised that MIA would result in brain volumetric changes subsequent to behavioural anomalies in the adult offspring with maternal exposure to Poly (I:C), for which abnormalities are normally pronounced by that time. In addition, the hypothesis that foetuses exposed to Poly (I:C) in early gestation stage would have increased expression level of apoptotic proteins of extrinsic types, namely Fas receptor, caspase-8 and the death effector caspase-3. This study found that, although male adult offspring with early maternal exposure to Poly (I:C) had an increase in raw whole brain volume, this was not significant when body weight was included as a covariable. However, prenatal exposure caused behavioural features similar to those reported in schizophrenia and autism such as prepulse inhibition deficits, increased anxiety-level and higher locomotor activity in response to amphetamine challenge. On the other hand, a marked augmentation in caspase-8 level without any significant changes in Fas or caspase-3 was observed in the adult hippocampus. No alterations in the expression of selected apoptotic proteins were found in the embryonic cortical cells. Overall the present studies suggested that acute exposure to infection during early fetal development causes a range of aberrations in brain anatomy, behaviour and biochemistry that are of relevance to the pathophysiology of schizophrenia and autism. The results suggest a potential involvement of synaptic apoptosis in cellular events underlying neurodevelopmental disorders.
published_or_final_version
Psychiatry
Master
Master of Philosophy
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Pascoal, Carlota Moutinho. "Immunological aspects of glycosylation: from aberrant to defective glycosylation." Master's thesis, 2017. http://hdl.handle.net/10362/27755.

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Glycosylation is crucial in many biological processes, like cell recognition, signaling and development. Many diseases present altered glycosylation and two extremes are cancer and congenital disorders of glycosylation (CDG), with aberrant and defective glycosylation, respectively. Sialic acids are glycans’ terminal sugars with an immunomodulatory role and when decreased, typically activate immune cells, as dendritic cells. Interestingly, both ST6Gal-I and its derived α2,6 sialylation are overexpressed in cancer. Here, we hypothesized that cancer cells secret functional ST6Gal-I that modulates immune cells’ glycosylation and their activity as a cancer immune evasion mechanism. Also interestingly, patients with PMM2-CDG (the most frequent CDG type) present immunological affectation. Here, we hypothesized that the PMM2-CDG-defective glycosylation observed also influences the function of immune cells. Therefore, the main goals of this study comprised the assessment of the immunological aspects of cancer cells and CDG glycosylation. Specifically, we intended to (1) study the expression and secretion of ST6Gal-I by colorectal cancer (CRC) cells and test its function in modulating immune cells activity; (2) develop a PMM2-CDG leukocyte cell line as a model to unravel patients’ immunity and to evaluate their response to mitogenic stimulation. Moreover, as PMM2-CDG have a profound impact in patients’ quality of life (QoL), patient and observer reported outcomes measures (PROMs and ObsROMs) were reviewed. These may integrate primary endpoints in clinical trials to find treatment to PMM2-CDG. Our data demonstrated that (1) CRC cells secret ST6Gal-I enzyme, however further work is needed to evaluate its role in immune modulation; (2) PMM2-CDG T cells have higher proliferation capacity and IFN-γ cytokine expression, in response to a mitogen as compared to the healthy control and (3) there are significant numbers of tools for future evaluation of PMM2-CDG patients’ and caregivers’ QoL. This study may contribute to better understand the glycan-related pathological mechanisms.
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Duursma, June. "Neutrophil cytoplasmic antibodies : their clinical associations and an improved method for their detection." Thesis, 1993. http://hdl.handle.net/10413/7360.

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The test for antineutrophil cytoplasmic antibodies (ANCA) was introduced into the author's laboratory in 1987. An improved indirect immunofluorescent method was developed, using a system which allows 16 instead of one serum sample to be screened on each microscope slide. The known disease associations of ANCA that have been explored include systemic vasculitis, renal limited vasculitis, chronic inflammatory bowel disease and HIV disease. In general the findings are similar to those which are emerging from other centres and confirm the value not only of the positivity but also the relevance of the intracellular disposition of the neutrophil cytoplasmic fluorescence in diagnosis. In this study 85% of patients with Wegener's granulomatosis were found to have C-ANCA. C, P and X-ANCA staining patterns were found in 57% of patients with ulcerative colitis. Forty one per cent of patients with symptomatic HIV have ANCA. Certain histological features such as neutrophil and vascular damage in invasive amoebiasis, and the established lytic effect of amoebae on neutrophils prompted the investigation of the possibility that ANCA may be generated in this disease. Seventy eight amoebiasis sera were screened and 98,70/0 gave a positive ANCA test with a pattern of fluorescence resembling that found in Wegener's granulomatosis. An ELISA test for specificity confirmed that, as in Wegener's granulomatosis, this amoebiasis-associated ANCA had proteinase 3 specificity. Of practical clinical importance is the fact that both HIV and amoebiasis are associated with a high level of ANCA positivity. These findings will need to be considered when ANCA tests are used in clinical decision making in an area where HIV disease and amoebiasis are endemic. A large number of normal volunteer blood donors have been tested and the false positivity rate of 0,5% confirms the specificity of the test.
Thesis (M.Med.)-University of Natal, Durban, 1993.
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Terrientes, S. Zilka I. "Study of the antigenicity of P. yoelii parasitized erythrocyte ghost antigens and their role in protection." Thesis, 1990. http://hdl.handle.net/10125/9440.

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Himes, Evan Robert. "The role of STAT3 in osteoclast mediated bone resorption." Thesis, 2014. http://hdl.handle.net/1805/4841.

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Indiana University-Purdue University Indianapolis (IUPUI)
Signal Transducer and Activator of Transcription 3 (STAT3) is known to be related to bone metabolism. Mutation of STAT3 causes a rare disorder in which serum levels of IgE are elevated. This causes various skeletal problems similar to osteoporosis. To examine the effect of STAT3 in the osteoclast, we obtained two osteoclast specific STAT3 knockout mouse models: one using the CTSK promoter to drive Cre recombinase and another using a TRAP promoter. Examination of these mice at 8 weeks of age revealed a decreased trabecular bone volume in CTSK specific STAT3 knockout mice along with a slight decrease in osteoclast number in both CTSK and TRAP specific STAT3 knockout females. We also noticed changes in bone mineral density and bone mechanical strength in females. These data suggest that STAT3 plays a part in the function of the osteoclast.
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McCain, Travis William. "Vitamin D Inhibits Expression of Protein Arginine Deiminase 2 and 4 in Experimental Autoimmune Encephalomoyelitis Model Of Multiple Sclerosis." Thesis, 2014. http://hdl.handle.net/1805/6018.

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Indiana University-Purdue University Indianapolis (IUPUI)
Multiple sclerosis (MS) is a disabling disease that afflicts an estimated two million people worldwide. The disease is characterized by degradation of the myelin sheath that insulates neurons of the central nervous system manifesting as a heterogeneous collection of symptoms. Two enzymes, protein arginine deaminases type 2 and 4 (PAD2 and PAD4) have been implicated to play an etiologic role in demyelination and neurodegeneration by catalyzing a post-translational modification of arginine peptide residues to citrulline. The pathogenesis of MS is poorly understood, though vitamin D deficiency is a well-associated risk factor for developing the disorder. Using the experimental autoimmune encephalomyelitis (EAE) model of MS we demonstrate vitamin D treatment to attenuate over-expression of PAD 2 and 4 in the brain and spine during EAE. In addition, we identify two molecules produced by peripheral immune cells, IFNɣ and IL-6, as candidate signaling molecules that induce PAD expression in the brain. We demonstrate vitamin D treatment to inhibit IFNɣ mediated up regulation of PAD2 and PAD4 both directly within the brain and by modulating PAD-inducing cytokine production by infiltrating immune cells. These results provide neuroprotective rational for the supplementation of vitamin D in MS patients. More importantly, these results imply an epigenetic link between vitamin D deficiency and the pathogenesis of MS that merits further investigation.
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Books on the topic "Immunological aspects of Neurocutaneous disorders"

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Clinical neuroimmunology: Multiple sclerosis and related disorders. Humana, 2010.

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Immunological and inflammatory disorders of the central nervous system. Butterworth-Heinemann, 1999.

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Conference on Neuroimmunophilins (1st 1999 Schlangengad, Germany). Immunophilins in the brain: FKBP Ligands: novel strategies for the treatment of neurodegenerative disorders. Prous Science, 2000.

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Skin in psychoanalysis. Karnac, 2007.

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Amor, Sandra. Autoimmunity to neuronal proteins in neurological disorders. Nova Science, 2011.

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1947-, Kaplan-Gouet C., and Salmon Charles 1925-, eds. Platelet immunology. Karger, 1988.

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F, Jackson William, ed. A colour atlas of allergic skin disorders. Wolfe Publishing Ltd., 1992.

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Mar, Pearl. Analysis of clonality and lineage of leukemic cell populations and monitoring of bone marrow transplantation using in situ hybridization and blotting methods. GSF-Forschungzentrum für Umwelt Und Gesundheit, 1991.

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Casanova, Jean-Laurent, Mary Ellen Conley, and Luigi Notarangelo. The year in human and medical genetics: Inborn errors of immunity I. Edited by New York Academy of Sciences. Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2011.

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Infectious behavior: Brain-immune connections in autism, schizophrenia, and depression. MIT Press, 2011.

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Book chapters on the topic "Immunological aspects of Neurocutaneous disorders"

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Kagaya, Ariyuki, and Shigeto Yamawaki. "Immunological Aspects of Mood Disorders: Interaction Between Cytokines and Intracellular Calcium Signaling." In Signal Transduction in Affective Disorders. Springer Japan, 1998. http://dx.doi.org/10.1007/978-4-431-68479-4_4.

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"General aspects of aetiology, diagnostics and therapy." In Neurocutaneous Disorders. Elsevier, 2016. http://dx.doi.org/10.1016/b978-3-437-24286-1.00001-0.

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Bhatt, Prakash. "Immunological Aspects in Pre-eclampsia." In Hypertensive Disorders in Pregnancy. Jaypee Brothers Medical Publishers (P) Ltd., 2007. http://dx.doi.org/10.5005/jp/books/10368_7.

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Kumagai, Naoko, Hiroaki Hayashi, Megumi Maeda, et al. "Immunological Effects of Silica and Related Dysregulation of Autoimmunity." In Autoimmune Disorders - Pathogenetic Aspects. InTech, 2011. http://dx.doi.org/10.5772/19218.

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Gupta, Somesh, Manoj Tembhre, Alpana Sharma, and Rehan Khan. "Clinical, Biochemical and Immunological Aspects of Vitiligo." In Pigmentary Disorders: A Comprehensive Compendium. Jaypee Brothers Medical Publishers (P) Ltd., 2014. http://dx.doi.org/10.5005/jp/books/12080_15.

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Tandon, Kokil. "Myasthenia Gravis: Clinical and Immunological Aspects." In Immunopathogenesis and Immune-based Therapy for Selected Autoimmune Disorders. InTech, 2017. http://dx.doi.org/10.5772/67684.

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Huang, Fang-Ping, and Susanne Sattler. "Regulatory T Cell Deficiency in Systemic Autoimmune Disorders – Causal Relationship and Underlying Immunological Mechanisms." In Autoimmune Disorders - Pathogenetic Aspects. InTech, 2011. http://dx.doi.org/10.5772/21297.

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Pachana, Nancy A. "2. Physical and biological aspects of ageing." In Ageing: A Very Short Introduction. Oxford University Press, 2016. http://dx.doi.org/10.1093/actrade/9780198725329.003.0002.

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‘Physical and biological aspects of ageing’ considers influences on longevity and the physical disorders commonly experienced at the end of life. It describes primary and secondary ageing and different biological theories of ageing—error and programme theories. Error theories (e.g. wear and tear theory, free radical theory, and somatic DNA damage theory) postulate that ageing and death are the result of environmental damage to the body over time. Programme theories (e.g. endocrine theory, immunological theory, and genetic theory (programmed longevity)) postulate that lifelong growth and development is genetically programmed to follow a pre-determined timeline. The ageing brain and body, and disease trajectories later in life are also considered.
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