Relevant bibliographies by topics / Unresponsiveness

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Unresponsiveness'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Unresponsiveness"

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Hurwitz, Trevor A. "Psychogenic Unresponsiveness." Neurologic Clinics 29, no. 4 (November 2011): 995–1006. http://dx.doi.org/10.1016/j.ncl.2011.07.006.

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Bernstein, R., and S. Futterer. "Venous unresponsiveness." Lancet 363, no. 9406 (January 2004): 368. http://dx.doi.org/10.1016/s0140-6736(04)15439-1.

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Sanders, Robert D., Giulio Tononi, Steven Laureys, Jamie W. Sleigh, and David S. Warner. "Unresponsiveness ≠ Unconsciousness." Anesthesiology 116, no. 4 (April 1, 2012): 946–59. http://dx.doi.org/10.1097/aln.0b013e318249d0a7.

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Consciousness is subjective experience. During both sleep and anesthesia, consciousness is common, evidenced by dreaming. A defining feature of dreaming is that, while conscious, we do not experience our environment; we are disconnected. Besides inducing behavioral unresponsiveness, a key goal of anesthesia is to prevent the experience of surgery (connected consciousness), by inducing either unconsciousness or disconnection of consciousness from the environment. Review of the isolated forearm technique demonstrates that consciousness, connectedness, and responsiveness uncouple during anesthesia; in clinical conditions, a median 37% of patients demonstrate connected consciousness. We describe potential neurobiological constructs that can explain this phenomenon: during light anesthesia the subcortical mechanisms subserving spontaneous behavioral responsiveness are disabled but information integration within the corticothalamic network continues to produce consciousness, and unperturbed norepinephrinergic signaling maintains connectedness. These concepts emphasize the need for developing anesthetic regimens and depth of anesthesia monitors that specifically target mechanisms of consciousness, connectedness, and responsiveness.
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Pepinsky, Hal. "Violence as unresponsiveness." Peace Review 4, no. 4 (December 1992): 75–80. http://dx.doi.org/10.1080/10402659208425684.

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Pinsker, M. Craig. "Unresponsiveness versus Unconsciousness." Anesthesiology 117, no. 5 (November 1, 2012): 1140. http://dx.doi.org/10.1097/aln.0b013e31826f8b9a.

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Jang, David H., and Lewis S. Nelson. "Woman With Unresponsiveness." Annals of Emergency Medicine 56, no. 2 (August 2010): 201–7. http://dx.doi.org/10.1016/j.annemergmed.2009.09.007.

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Lee, Tommy Kwok Ping, Abdul Karim Bin Kitchell, Axel Yuet Chung Siu, and Ngan Kwan Chen. "Validation of the Full Outline of Unresponsiveness score coma scale in patients clinically suspected to have acute stroke in the emergency department." Hong Kong Journal of Emergency Medicine 24, no. 5 (September 2017): 230–36. http://dx.doi.org/10.1177/1024907917724723.

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Introduction: The Full Outline of Unresponsiveness score coma scale is a recently introduced coma scale. The objectives of this study were to assess the interrater reliability of the Full Outline of Unresponsiveness score coma scale when physicians and nurses in the emergency department apply the Full Outline of Unresponsiveness score on patients clinically suspected to have acute stroke and to look for any association between Full Outline of Unresponsiveness score coma scale and in-hospital mortality. Methods: Prospective study of 105 patients clinically suspected to have acute stroke recruited in an emergency department in a 4-month period. The Full Outline of Unresponsiveness score coma scale and Glasgow Coma Scale of each patient were assessed by one doctor and one nurse independently. The interrater reliability between physicians and nurses using the Full Outline of Unresponsiveness score and Glasgow Coma Scale score was assessed. The association between the Full Outline of Unresponsiveness score coma scale and in-hospital mortality was analysed using logistic regression, controlled for age, sex and diagnosis. Results: Full Outline of Unresponsiveness score had a good interrater reliability when applied to patients suspected to have acute stroke (kappa = 0.742, 95% confidence interval = 0.626–0.858). This was comparable to Glasgow Coma Scale score with a kappa = 0.796 (95% confidence interval = 0.694–0.898). For every 1-point increase in Full Outline of Unresponsiveness score coma scale, a reduction in in-hospital mortality was observed with an odds ratio of 0.76 (95% confidence interval = 0.63–0.91, p = 0.003), controlled for age, sex and diagnosis. Conclusion: The Full Outline of Unresponsiveness score may be a tool that can be used by emergency department doctors and nurses in assessing clinical stroke patients.
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Ben-Noun, Liubov. "Unresponsiveness to Nifedipine Treatment." DICP 25, no. 1 (January 1991): 99. http://dx.doi.org/10.1177/106002809102500119.

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Perkins, Herbert A. "Transfusion-Induced Immunologic Unresponsiveness." Transfusion Medicine Reviews 2, no. 4 (December 1988): 196–203. http://dx.doi.org/10.1016/s0887-7963(88)70045-0.

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Rapoport, M. J., A. Jaramillo, D. Zipris, A. H. Lazarus, D. V. Serreze, E. H. Leiter, P. Cyopick, J. S. Danska, and T. L. Delovitch. "Interleukin 4 reverses T cell proliferative unresponsiveness and prevents the onset of diabetes in nonobese diabetic mice." Journal of Experimental Medicine 178, no. 1 (July 1, 1993): 87–99. http://dx.doi.org/10.1084/jem.178.1.87.

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Beginning at the time of insulitis (7 wk of age), CD4+ and CD8+ mature thymocytes from nonobese diabetic (NOD) mice exhibit a proliferative unresponsiveness in vitro after T cell receptor (TCR) crosslinking. This unresponsiveness does not result from either insulitis or thymic involution and is long lasting, i.e., persists until diabetes onset (24 wk of age). We previously proposed that it represents a form of thymic T cell anergy that predisposes to diabetes onset. This hypothesis was tested in the present study by further investigating the mechanism responsible for NOD thymic T cell proliferative unresponsiveness and determining whether reversal of this unresponsiveness protects NOD mice from diabetes. Interleukin 4 (IL-4) secretion by thymocytes from > 7-wk-old NOD mice was virtually undetectable after treatment with either anti-TCR alpha/beta, anti-CD3, or Concanavalin A (Con A) compared with those by thymocytes from age- and sex-matched control BALB/c mice stimulated under identical conditions. NOD thymocytes stimulated by anti-TCR alpha/beta or anti-CD3 secreted less IL-2 than did similarly activated BALB/c thymocytes. However, since equivalent levels of IL-3 were secreted by Con A-activated NOD and BALB/c thymocytes, the unresponsiveness of NOD thymic T cells does not appear to be dependent on reduced IL-2 secretion. The surface density and dissociation constant of the high affinity IL-2 receptor of Con A-activated thymocytes from both strains are also similar. The patterns of unresponsiveness and lymphokine secretion seen in anti-TCR/CD3-activated NOD thymic T cells were also observed in activated NOD peripheral spleen T cells. Exogenous recombinant (r)IL-2 only partially reverses NOD thymocyte proliferative unresponsiveness to anti-CD3, and this is mediated by the inability of IL-2 to stimulate a complete IL-4 secretion response. In contrast, exogenous IL-4 reverses the unresponsiveness of both NOD thymic and peripheral T cells completely, and this is associated with the complete restoration of an IL-2 secretion response. Furthermore, the in vivo administration of rIL-4 to prediabetic NOD mice protects them from diabetes. Thus, the ability of rIL-4 to reverse completely the NOD thymic and peripheral T cell proliferative defect in vitro and protect against diabetes in vivo provides further support for a causal relationship between this T cell proliferative unresponsiveness and susceptibility to diabetes in NOD mice.
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Dissertations / Theses on the topic "Unresponsiveness"

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Losson, B. J. "Immunological unresponsiveness to gastrointestinal nematodes." Thesis, University of Cambridge, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372886.

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Mahmood, Khalid Hassan. "The immunological unresponsiveness of badgers to mycobactera." Thesis, University College London (University of London), 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319747.

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Rankin, Alasdair Menzies. "An investigation of CD28/B7 family binding interactions and costimulation, using immunoglobulin fusion proteins." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360469.

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Tavernor, Angela Susan. "The immune unresponsiveness of the lamb and infection with Haemonchus contortus." Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292862.

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Khalaf, Rana. "Nontypeable Haemophilus influenzae-induced inflammation, corticosteroids unresponsiveness and functional polarisation in COPD alveolar macrophages." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/nontypeable-haemophilus-influenzaeinduced-inflammation-corticosteroids-unresponsiveness-and-functional-polarisation-in-copd-alveolar-macrophages(bcbe33db-3d70-4c0b-b39d-805d448ef693).html.

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COPD is a chronic inflammatory disease of the airways where many patients have recurrent lower airway bacterial infection, most commonly nontypeable Haemophilus influenzae (NTHi). Corticosteroids are commonly used anti-inflammatory drugs in COPD with limited clinical benefit. Previous studies focused on corticosteroid responsiveness in COPD did not consider the role of airway NTHi infection. Alveolar macrophages are the main inflammatory cells in COPD pathogenesis, a shift in their phenotype was highlighted in COPD patients. Some bacteria can modify alveolar macrophage phenotype to persist in the lower airways. I have optimised a clinically relevant in vitro model of NTHi infection; human alveolar macrophages were stimulated with an increasing load of live NTHi clinical isolate (R2846). NTHi provoked time-dependent release of TNF-α, IL-6, CXCL8 and IL-10 from alveolar macrophages, which was correlated with bacterial growth, lysis and phagocytosis in the model. Furthermore, NTHi load was inversely correlated with IL-10 release. These findings suggest that NTHi infection is a dynamic inflammatory process in human alveolar macrophages and pointed to the possible role of IL-10 in the NTHi persistence in the lower airways. NTHi-induced cytokines in alveolar macrophages showed reduced corticosteroid responsiveness, CXCL8 was particularly corticosteroid unresponsive cytokine. NTHi-induced glucocorticoid receptor (GR) phosphorylation at ser 226 residue, which would encourage GR nuclear exportation. This might be one possible mechanism of reduced corticosteroid response in the model. In line with the latter finding, NTHi impaired the corticosteroid-induced GR nuclear localisation, which was partially reversed by p38 MAPK inhibitor (BIRB-796). These results suggest the role of NTHi in corticosteroid unresponsiveness in COPD alveolar macrophages. NTHi-induced cytokine release in alveolar macrophages was mediated by NF-κB, p38 and ERK MAPK pathways. Combination of corticosteroid (dexamethasone) with p38 and ERK MAPK inhibitors (BIRB-796 and AZD6244 respectively) showed a potential synergistic anti-inflammatory effect in the model. Therefore, inhibitors of MAPK pathways might serve as future anti-inflammatory therapies in NTHi-infected COPD patients. NTHi in vitro infection caused upregulation of the pro-inflammatory (TNF-α, CXCL8, CD38) and the anti-inflammatory (IL-10) markers’ mRNA levels in COPD alveolar macrophages. Meanwhile, NTHi downregulated the antigen-presentation molecule (HLA-DR) and the scavenger receptors (CD14, CD36, CD163 and CD206) mRNA levels in COPD alveolar macrophages. Moreover, sputum macrophages from NTHi-infected stable COPD patients showed lower mRNA levels of CD36 and HLA-DR. These findings suggest that the NTHi modification of alveolar macrophage functions, especially antigen presentation and efferocytosis, might be a possible mechanism of NTHi chronic infection and COPD disease progression.
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Bell, Yvonne Louise. "An investigation into the induction of specific immunological unresponsiveness using donor major histompatibility complex antigens." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386871.

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Quigley, R. L. "Investigation of the mechanism of induction of immunologic unresponsiveness to renal allografts by blood transfusion." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233514.

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Madsen, Joren Christian. "A genetic analysis of antigen-induced specific unresponsiveness using recipient cells transfected with donor MHC genes." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302818.

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Fry, Jeremy. "Delivery of a donor MHC class I gene using a recombinant adenovirus to induce immunological unresponsiveness." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343471.

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Niimi, Masanori. "An investigation to determine the ability of allogeneic resting B cells to induce specific unresponsiveness in vivo." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244813.

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Books on the topic "Unresponsiveness"

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Fox, Susan H. Wakeful Unresponsiveness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0029.

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NMDA receptor encephalitis is a member of the growing group of antibody-mediated neurological syndromes that can present acutely to neurological services. In the past, these entities were undoubtedly misdiagnoses as viral encephalitis or schizophrenia. The identification of the NMDA receptor antibody and a stereotypical phenotype has greatly improved the chance of a diagnosis in these patients. Furthermore, there is good evidence for the use of early immunotherapy, which may need to be sustained and increased in resistant cases that may still achieve a full recovery. The presence of an ovarian teratoma must be excluded in young females, although young males and females may also be affected in the absence of an underlying tumor.
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Bonavida, Benjamin, and Ganji Purnachandra Nagaraju. Breaking Tolerance to Pancreatic Cancer Unresponsiveness to Chemotherapy. Elsevier Science & Technology Books, 2019.

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Breaking Tolerance to Pancreatic Cancer Unresponsiveness to Chemotherapy. Elsevier, 2019. http://dx.doi.org/10.1016/c2018-0-02682-1.

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Matosevic, Sandro. Breaking Tolerance to Unresponsiveness to Immunotherapy by Natural Killer Cells. Elsevier Science & Technology, 2020.

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Matosevic, Sandro. Breaking Tolerance to Unresponsiveness to Immunotherapy by Natural Killer Cells. Elsevier Science & Technology Books, 2020.

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Massimini, Marcello, and Giulio Tononi. Brain Islands. Translated by Frances Anderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198728443.003.0003.

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This chapter examines the clinical problem of detecting consciousness in brain-injured patients who emerge from coma in a state of behavioral unresponsiveness. Intensive care medicine is artificially producing, as a by-product of saving many lives, brains that may remain isolated, split, or fragmented. In extreme cases, large cortical islands or an archipelago of islands may survive totally dissociated from the world outside. Can these islands sustain consciousness? Does it feel like anything to be a big chunk of isolated human cortex? Scientific and philosophical doubts aside, we need to urgently address this question. The text underscores the necessity and difficulty of developing brain-based objective measures of consciousness, which are independent of sensory processing and motor behavior.
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Niaudet, Patrick, and Alain Meyrier. Minimal change disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0055_update_001.

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Minimal change disease is the most common cause of nephrotic syndrome in childhood but is not rare in adults. The factors altering permeability of the glomerular filtration barrier are not known, but podocyte structure is significantly altered in the condition and it seems certain that this cell is the target of whatever factors are responsible for the condition. It is still not clear that it is immunologically mediated and many of the agents used to treat it have direct effects on the podocyte. The differential diagnosis includes any other disease causing nephrotic syndrome, and a renal biopsy narrows this down. In children, steroid unresponsiveness is often used as a diagnostic test, and consideration of genetic or other pathologies reserved for patients who show no or poor steroid responsiveness.
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Alvarez, Maria, and Clayton Littlejohn, eds. When Ignorance is No Excuse. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198779667.003.0003.

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The chapter argues that the best non-skeptical accounts of moral responsibility acknowledge that factual ignorance and mistake will diminish moral responsibility in a way that moral ignorance and mistake will not. That is because factual ignorance is often non-culpable so long as it meets certain merely procedural epistemic standards but the same is not true of moral ignorance. The chapter’s argument is that the assumption that it is gets the standards of culpability for moral ignorance wrong, and that the mistake is encouraged by the thought that culpability in general requires an instance of known wrongdoing: that acting wrongly requires de dicto unresponsiveness to one’s obligations at some stage. The chapter denies this and concludes that, therefore, ignorance and mistaken belief are indeed often perfectly good excuses—but far less often than some philosophers claim.
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Drislane, Frank W., Susan T. Herman, and Peter W. Kaplan. Convulsive Status Epilepticus. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0020.

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Generalized convulsive status epilepticus (GCSE) is a serious neurologic illness causing unresponsiveness, major physiologic disturbances, risk of injury and, if prolonged enough, neuronal damage. Causes are many, and the outcome often depends as much on the etiology as on the epileptic seizure itself. Several anti-seizure medications are used in treatment of GCSE, but some cases continue electrographically when clinical convulsions cease (nonconvulsive SE), and EEG is essential in their diagnosis. About 20% of cases become refractory to initial treatment, and the EEG becomes even more crucial in diagnosis and management. This chapter also covers other forms of SE with significant motor manifestations including: focal motor status (including epilepsia partialis continua); myoclonic status, which includes some relatively benign forms as well as some with a very poor prognosis; and clonic and tonic status. It reviews the many different EEG findings in those forms of status, and the use of EEG in their treatment and management, especially in prolonged cases.
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Posner, Jerome B., Clifford B. Saper, Nicholas D. Schiff, and Jan Claassen. Plum and Posner's Diagnosis and Treatment of Stupor and Coma. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190208875.001.0001.

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This text is an update of a classic work on diagnosing the cause of coma, with the addition of new sections on the treatment of comatose patients. The first chapter provides an up-to-date review on the brain mechanisms that maintain a conscious state in humans and how lesions that damage these mechanisms cause loss of consciousness or coma. The second chapter reviews the neurological examination of the comatose patient, which provides the basis for determining whether the patient is suffering from a structural brain injury causing the coma or from a metabolic disorder of consciousness. The third and fourth chapters review the pathophysiology of structural lesions causing coma and the specific disease states that result in coma. Chapter 5 is a comprehensive treatment of the many causes of metabolic coma. Chapter 6 review psychiatric causes of unresponsiveness and how to identify and treat them. Chapters 7 and 8 review the overall emergency treatment of comatose patients, followed by the treatment of specific causes of coma. Chapter 9 examines the long-term outcomes of coma, including the minimally conscious state and the persistent vegetative state, how they can be distinguished, and their implications for eventual useful recovery. Chapter 10 reviews the topic of brain death, the standards for examination of a patient that are required to make the determination of brain death, and the ethics of diagnosis and treatment of patients who, by definition, have no way to approve of or communicate about their wishes.
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Book chapters on the topic "Unresponsiveness"

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Rother, K., and P. Terness. "Immunologic Measures: Unresponsiveness or Tolerance." In Cancer in Organ Transplant Recipients, 161–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75991-8_16.

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Miller, Richard G. "Induction of Immunological Unresponsiveness in the Adult Animal." In Tissue Engineering, 209–13. Boston, MA: Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4615-8186-4_20.

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Kaufman, M., F. Andris, and O. Leo. "Theoretical Insight into Antigen-Induced T-Cell Unresponsiveness." In Theoretical and Experimental Insights into Immunology, 93–115. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76977-1_7.

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Finke, James H., and Mahesh Goel. "T-cell Unresponsiveness in Renal Cell Carcinoma Patients." In Clinical Management of Renal Tumors, 115–30. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-149-3_7.

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Scott, David W. "Multiple mechanisms of immunologic tolerance: Novel approaches for unresponsiveness." In Advances in Experimental Medicine and Biology, 209–20. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4613-0331-2_20.

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Tada, T., S. Kubo, and T. Nakayama. "Self-Tolerance: Multiple Strategies for Peripheral Unresponsiveness of T Cells." In New Trends in Allergy IV, 359–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60419-5_63.

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Lamb, J. R., and E. D. Zanders. "The Induction of Antigen Specific Unresponsiveness in Cloned T Lymphoctyes." In Immune Regulation, 51–59. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-4996-2_5.

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Lamb, J. R., Marc Feldmann, E. D. Zanders, and P. C. L. Beverley. "Antigen-T Lymphocyte Interactions in the Induction of Functional Unresponsiveness." In Human T Cell Clones, 309–15. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-4998-6_28.

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Monaco, Anthony P. "Current Status of Induction of Specific Unresponsiveness to Organ Allografts." In Chronic Renal Disease, 523–27. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4826-9_53.

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Heissmeyer, Vigo, Fernando Maciá, Rajat Varma, Sin-Hyeog Im, Francisco García-Cozar, Heidi F. Horton, Michael C. Byrne, et al. "A Molecular Dissection of Lymphocyte Unresponsiveness Induced by Sustained Calcium Signalling." In Novartis Foundation Symposia, 165–79. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/047002139x.ch11.

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Conference papers on the topic "Unresponsiveness"

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Miklos, Walter, Karla Pelivan, Christian Kowol, Rita Dornetshuber-Fleiss, Melanie Spitzwieser, Margit Cichna-Markl, Gunda Köllensperger, Bernhard Keppler, Walter Berger, and Petra Heffeter. "Abstract 5461: Triapine-mediated ABCB1 induction via PKC induces widespread therapy unresponsiveness but is not underlying acquired triapine resistance." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5461.

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Kudo-Saito, Chie, Takahiro Miyamoto, Mami Kawamura, Yamato Ogiwara, and Kazunori Aoki. "Abstract 708: Increase of senescent mesenchymal stromal/stem cells is predictive of unresponsiveness to the treatment with immune checkpoint inhibitors." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-708.

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Muller, Ittai, Marry Lin, Willem Lems, Marieke Ter Wee, Jacqueline Cloos, Yehuda Assaraf, Gerrit Jansen, and Robert De Jonge. "THU0063 PRE-MRNA SPLICING ALTERATIONS IN FOLYLPOLYGLUTAMATE SYNTHETASE IN BLOOD CELLS OF EARLY RHEUMATOID ARTHRITIS PATIENTS ARE ASSOCIATED WITH UNRESPONSIVENESS TO METHOTREXATE." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3215.

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Semeraro, N., A. Errori, B. Casali, M. B. Dontati, and A. Mantovani. "DEFECTIVE GENERATION OF PROCOAGULANT ACTIVITY BY TUMOR-ASSOCIATED MACROPHAGES EXPOSED TO DIFFERENT STIMULI." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643665.

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Mononuclear phagocytes, an integral part of the lymphoreticular infiltrate of human and experimental tumors, might contribute to fibrin deposition within malignant tissues through the production of procoagulant activity (PCA). We have studied the PCA of tumor-associated macrophages (TAM) in two poorly immunogenic, metastatic murine sarcomas (mFS6 and MN/MCA1); peritoneal macrophages (PM)from tumor-bearing and control animals were also studied, as reference cell populations. TAM were prepared from disaggregated tumor tissue and PM from ‘lavage’ fluid by adherence to plastic.PCA was evaluated by a one-stage clotting assay immediately after isolation (basal PCA) and following in vitro stimulatio.Basal PCA was very low(<1 u/104 M) inall cellpreparations. Exposure of PM from both normal and tumor-bearing animals to endotoxin (S. enteritidis LPS, 1 ug/ml f..), phorbol myristate acetate (PMA,0. ug/ml) or the chemotactic peptide FMLP(10-7 M) resulted in a 10-,7- and 3-fold increase of PCA respectively. In contrast TAM from mFS6 and MN/MCA1 consistently failed to generate PCAin response to different concentrationsof the same stimuli. Treatment of TAM with aspirin (10-3M) did not affect the cell unresponsiveness. Fluorescence microscopy showed that almost all PM were stain ed with fluorescein isothiocyanate (FITC)-LPS, while 10% of the TAM were stained. Moreover binding studies demonstrated that TAM had a loyer number of specific binding sites for phorbol esters than PM. These data suggest that the defective responsiveness of TAM to endotoxin, PMA and, possibly, to FMLP is due to the lack or very low expression of binding sites for these agents on the cell surface. The tumor environment may orient the functional status of in situ macrophages in a sense less favourable to the host.
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Szigeti, Mónika Veronika. "BURNOUT PREVENTION WITH PSYCHOEDUCATION IN TEACHERS." In International Conference on Education and New Developments. inScience Press, 2021. http://dx.doi.org/10.36315/2021end044.

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Our research aims at prevention of burnout, which can be a protective factor in preventing career abandonment and can contribute to creating and maintaining a positive workplace climate. It also promotes the mental well-being and resilience of teachers and students. Therefore, burnout of teachers is especially important in Hungary, as the gradually increasing professional and administrative burden, the lack of social esteem, as well as the changed learning-teaching environment and the methodological shortcomings of general teacher training significantly increase the risk of burnout. In our research, the staff of the Somogy County Educational Service Center has been involved, mainly special education teachers. The 116-person sample has been conducted with a version of the Maslach Burnout Inventory developed for educators. In our presentation, the test results are presented. According to our findings, out of the three subscales of the subjects' questionnaire, the highest scores were achieved in the Emotional Exhaustion subscale and the lowest in the Depersonalization subscale. However, the emotional exhaustion subscale did not indicate a high burnout value in the study population. The correlations of burnout risk with age and time spent as a teacher has been also analyzed. Problem-focused and change-oriented psychological counseling models are attracting interest in the international literature today (Egan, 2010). By strengthening resilience and supporting a sense of growth, consultation techniques work to strengthen effective interpersonal communication and help the individual plan constructively for the future (Bonanno, 2004, 2005; Kelley, 2005; Linley & Joseph, 2005; Litz, 2005; Maddi, 2005). All of this are relevant to our research because we plan to provide burnout prevention psychoeducation counseling programs to educators. The literature also mentions the phenomenon of learned helplessness, which has its roots in childhood and is a breeding ground for both depression and burnout (Seligman,1991). Learned inertia can influence members of the helping professions toward passivity (paralysis, loss of control, hopelessness, unresponsiveness) and is therefore particularly burdensome for the individual, along with the challenges of helping professions. Results of our research shed light on the burnout level of special educators, personality traits important for coping and related burnout prevention (e.g., empathy, psychological immune competence) and the applied coping mechanisms that guide burnout prevention psychoeducation as a comprehensive concept.
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Reports on the topic "Unresponsiveness"

1

Oreopoulos, Philip, and Uros Petronijevic. The Remarkable Unresponsiveness of College Students to Nudging And What We Can Learn from It. Cambridge, MA: National Bureau of Economic Research, July 2019. http://dx.doi.org/10.3386/w26059.

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