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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Nair, Sharath S., Anilkumar Surendran, Rajmohan B. Prabhakar, and Meer M. Chisthi. "Comparison between FOUR score and GCS in assessing patients with traumatic head injury: a tertiary centre study." International Surgery Journal 4, no. 2 (January 25, 2017): 656. http://dx.doi.org/10.18203/2349-2902.isj20170209.

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Background: Head injuries are a major cause of mortality and morbidity across the world. Effective initial assessment and early intervention is of importance in patients with traumatic brain injury, so as to ensure the maximum favorable outcome. Glasgow Coma Scale is the widely accepted scale to assess severity in head injury patients, albeit with many inadequacies. The objective of this study was to test the validity of full outline of unresponsiveness score, an alternate tool, in assessing severity in patients with traumatic brain injury.Methods: This was a descriptive study, conducted on 69 patients admitted to the general surgical and neuro-surgical wards of Government Medical College, Trivandrum, India with traumatic head injury. For all these patients, full outline of unresponsiveness score and Glasgow Coma Scale were calculated at the time of presentation and serially thereafter. The predictive value of full outline of unresponsiveness score as well as its correlation with Glasgow Coma Scale was studied.Results: A statistically significant correlation was found between full outline of unresponsiveness score and Glasgow Coma Scale in estimating the severity of head injury. Also Full Outline of unresponsiveness score was able to furnish better details about the neurological status of trauma patients.Conclusions: As per the results, it can be concluded that the full outline of unresponsiveness score can be applied as an ideal tool to evaluate consciousness levels and patients’ status in patients with traumatic head injury. It can be used as the ideal replacement for Glasgow Coma Scale.
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12

Huchet, R. "Hapten-specific unresponsiveness in mice." Annales de l'Institut Pasteur / Immunologie 137 (January 1986): 273–81. http://dx.doi.org/10.1016/s0771-050x(86)80046-8.

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13

Haurowitz, Felix. "IMMUNOLOGICAL UNRESPONSIVENESS AND AUTOANTIBODY FORMATION." Annals of the New York Academy of Sciences 124, no. 1 (December 16, 2006): 50–55. http://dx.doi.org/10.1111/j.1749-6632.1965.tb18941.x.

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14

Scott, D. W., J. E. Ales-Martinez, J. H. Chace, N. J. LoCascio, L. Silver, and G. L. Warner. "Models of B-cell Unresponsiveness." Cold Spring Harbor Symposia on Quantitative Biology 54 (January 1, 1989): 899–905. http://dx.doi.org/10.1101/sqb.1989.054.01.105.

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15

Rao, T. H., L. B. Schneider, and Y. Lupyan. "Transient Unresponsiveness in the Elderly." Archives of Neurology 51, no. 7 (July 1, 1994): 644. http://dx.doi.org/10.1001/archneur.1994.00540190018007.

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16

Haimovic, Itzhak C. "Transient Unresponsiveness in the Elderly." Archives of Neurology 49, no. 1 (January 1, 1992): 35. http://dx.doi.org/10.1001/archneur.1992.00530250039013.

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17

Wood, Kathryn J., Nick D. Jones, Andrew R. Bushell, and Peter J. Morris. "Alloantigen–induced specific immunological unresponsiveness." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1409 (May 29, 2001): 665–80. http://dx.doi.org/10.1098/rstb.2001.0840.

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When the immune system encounters alloantigen it can respond in any one of a number of different ways. The choice that is made will take into account factors such as where, when and how the contact with the alloantigen takes place, as well as the environmental conditions that prevail at the time the alloantigen is encountered. Alloantigen administration before transplantation either alone or in combination with therapeutic agents that modulate the functional activity of the responding leucocytes can be a powerful way of inducing specific unresponsiveness to alloantigens in vivo .The molecular mechanisms that influence the way the outcome of the immune response to alloantigen develops, either activation or unresponsiveness to the triggering antigen, hold the key to our ability to manipulate the immune system effectively by exposing it to donor antigen for therapeutic purposes. This review will focus on alloantigen–induced immunological unresponsiveness and how insights into the mechanisms of unresponsiveness have driven the development of novel tolerance–induction strategies that show promise for translation into the clinic in the future.
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18

HUCHET, R., and D. GRANDJON. "Hapten-Specific Unresponsiveness in Mice." Scandinavian Journal of Immunology 21, no. 4 (April 1985): 337–43. http://dx.doi.org/10.1111/j.1365-3083.1985.tb01439.x.

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19

Suh, Jungyo, Hyeong Dong Yuk, Chang Wook Jeong, Cheol Kwak, Hyeon Hoe Kim, and Ja Hyeon Ku. "Pyuria as a Predictive Marker of Bacillus Calmette–Guérin Unresponsiveness in Non-Muscle Invasive Bladder Cancer." Journal of Clinical Medicine 10, no. 17 (August 24, 2021): 3764. http://dx.doi.org/10.3390/jcm10173764.

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This study aims to investigate the clinical role of preoperative pyuria for predicting bacillus Calmette–Guérin (BCG) unresponsiveness in non-muscle invasive bladder cancer (NMIBC). We performed a logistic regression analysis on 453 patients with NMIBC who were treated with BCG immunotherapy after a transurethral resection of bladder tumours, to evaluate predictive factors of BCG unresponsiveness. We also analysed univariate and multivariable survival data to estimate the prognostic impact of pyuria. Of the total study population, 37.6% (170/453) of patients had BCG unresponsiveness. A multivariable logistic regression analysis revealed that a history of upper urinary tract cancer (odds ratio (OR): 1.86, 95% confidence interval (CI): 1.04–3.32, p-value = 0.035) and the presence of pyuria (OR: 1.51, 95% CI: 1.01–2.27, p = 0.047) and tumour multiplicity (OR: 1.80, 95% CI: 1.18–2.75, p-value < 0.001) were significant predictors of BCG unresponsiveness. A Cox proportional hazards analysis model showed that pyuria was a significant prognostic factor for progression-free survival (hazard ratio: 4.51, 95% CI: 1.22–16.66, p = 0.024). A history of upper urinary tract cancer and the presence of pyuria and tumour multiplicity are predictive markers of BCG unresponsiveness. For patients with NMIBC who have preoperative pyuria, treatment using BCG should be considered cautiously.
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20

Sevimli Dikicier, B. "Topical treatment of acne vulgaris: efficiency, side effects, and adherence rate." Journal of International Medical Research 47, no. 7 (May 24, 2019): 2987–92. http://dx.doi.org/10.1177/0300060519847367.

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Objective Adherence is a problem in the topical treatment of acne. This study was designed to evaluate the efficiency of current topical treatment and adherence in patients. Methods Patients with acne vulgaris who had recently been prescribed a topical therapy were selected. A dermatologist-directed questionnaire was completed. Demographic data, acne severity, treatment and the manner of use, side effects, and reason for discontinuation were recorded. Results A total 250 patients were included, 178 female (71.2%) and 72 male (28.8%) participants, mean age was 18.6 ± 2.8 years. Of 250 patients, 114 (45.6%) had given up therapy for two reasons: unresponsiveness in 71 (62.3%) and side effects in 43 (37.7%) patients. For antibacterial treatments, the rate of unresponsiveness was higher but the rate of side effects was lower. Discontinuation owing to unresponsiveness was higher in patients with severe acne. Side effects were higher in patients with comedonal-type acne. The lowest rates of side effects and discontinuation were among every-other-night users. Conclusion In this study, patients with acne gave up treatment owing to side effects and unresponsiveness, which reduced the treatment efficiency.
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21

Remuzzi, G., M. Noris, A. Benigni, O. Imberti, M. H. Sayegh, and N. Perico. "Thromboxane A2 receptor blocking abrogates donor-specific unresponsiveness to renal allografts induced by thymic recognition of major histocompatibility allopeptides." Journal of Experimental Medicine 180, no. 5 (November 1, 1994): 1967–72. http://dx.doi.org/10.1084/jem.180.5.1967.

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Recent in vitro studies have documented that thromboxane (Tx)A2 induces thymocyte apoptosis by acting on specific receptors abundantly expressed on the surface of immature T lymphocytes. No information is available on the in vivo relevance of this observation in development of self- or acquired tolerance. We and others have previously documented that injection of donor cells into adult thymus of experimental animals induced specific systemic unresponsiveness to allografts in the rat and mouse models. More recently, we have shown that intrathymic injection of synthetic class II major histocompatibility complex (MHC) allopeptides resulted in donor-specific unresponsiveness to renal allografts. The induction of unresponsiveness was abrogated by recipient thymectomy within the first week. We now report the effect of TxA2 blockade on acquired thymic tolerance to renal allografts induced by intrathymic injection of synthetic class II MHC allopeptides in the Wistar-Furth (WF) to Lewis rat strain combination. Administration of the TxA2 receptor blocker prior to transplantation or 2 wk postengraftment completely abrogated the unresponsive state. In addition, inhibiting the TxA2-forming enzyme by aspirin or dexamethasone also abolished the induction of acquired thymic tolerance. Evidence is also provided for a critical "dose" of peptides to be injected into the thymus to induce systemic unresponsiveness to renal allografts. These data, coupled with observations that activated peripheral T cells can circulate through the thymus, provide evidence that TxA2/TxA2 receptor interaction in the thymic microenvironment, leading to anergy/programmed cell death of activated T cells, may play an important role in the development of acquired unresponsiveness in vivo.
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22

van Ree, Ronald. "Sustained unresponsiveness in peanut oral immunotherapy." Lancet 394, no. 10207 (October 2019): 1392–93. http://dx.doi.org/10.1016/s0140-6736(19)31816-1.

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23

CORRIGAN, C. J. "Glucocorticoid unresponsiveness in severe ulcerative colitis." Gut 45, no. 3 (September 1, 1999): 324–25. http://dx.doi.org/10.1136/gut.45.3.324.

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24

Papageorgiou, Marina, Grigorios Theodosiou, and Ioanna Mandekou-Lefaki. "Eruptive syringomas: unresponsiveness to oral isotretinoin." International Journal of Dermatology 56, no. 2 (November 2, 2016): e38-e39. http://dx.doi.org/10.1111/ijd.13444.

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25

Sundar, Shyam, Anup Singh, and Om Prakash Singh. "Strategies to Overcome Antileishmanial Drugs Unresponsiveness." Journal of Tropical Medicine 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/646932.

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In the absence of effective vector control measures and vaccines against leishmaniasis, effective chemotherapy remains the mainstay of treatment. As the armoury of antileishmanial drugs is limited, strategies should be made to target the emergence of drug resistance. The loss of efficacy of antimonials such as sodium stibogluconate in the Indian subcontinent which has been the mainstay of treatment for more than six decades has raised concern to save the other drugs. In the current review, we highlight various steps which could be implemented to halt the increasing unresponsiveness of drugs such as monitoring of therapy in the form of rational dosing and duration of treatment, understanding the mechanism of action of the drugs and drug resistance, identification of markers of resistance, distribution of drugs free of cost, evolution of effective combination therapy and immunotherapy, and proper management of HIV/VL coinfection and post-kala-azar dermal leishmaniasis (PKDL). Strong support from governmental agencies and local communities in the form of education and orientation programmes for feasibility of implementing these strategies and affordability within the context of their health systems is needed in controlling and preventing leishmaniasis.
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26

Hart, Carol S., Stephen M. Rosenthal, Susan Shaw-Reines, Selna L. Kaplan, and Melvin M. Grumbach. "AURENOLEUKUDYSTROPHY MAY RESEMBLE FAMILIAL ACTH UNRESPONSIVENESS." Pediatric Research 21, no. 4 (April 1987): 248A. http://dx.doi.org/10.1203/00006450-198704010-00484.

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27

Bashir, I., V. Samuel, and S. El-Refee. "G441(P) Responding to hormone unresponsiveness." Archives of Disease in Childhood 99, Suppl 1 (April 1, 2014): A184. http://dx.doi.org/10.1136/archdischild-2014-306237.423.

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28

Seppälä, I. J. T. "HAPTEN-CARRIER RELATIONSHIPS IN IMMUNOLOGICAL UNRESPONSIVENESS." Acta Pathologica Microbiologica Scandinavica Section B Microbiology and Immunology 82B, no. 4 (August 15, 2009): 567–76. http://dx.doi.org/10.1111/j.1699-0463.1974.tb02367.x.

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29

Imamura, Masayuki, Yasuaki Hattori, Osamu Nishida, Toyohiko Honda, Yutaka Shimada, Tokiharu Miyahara, Takashi Wagata, Nobuo Baba, and Takayoshi Tobe. "Unresponsiveness of Insulinoma Cells to Secretin." Pancreas 5, no. 4 (July 1990): 467–73. http://dx.doi.org/10.1097/00006676-199007000-00015.

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30

Mohammed, Kader N. "Unresponsiveness to Etretinate during Anticonvulsant Therapy." Dermatology 185, no. 1 (1992): 79. http://dx.doi.org/10.1159/000247415.

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31

Adcock, Ian M., Pai-Chien Chou, Andrew Durham, and Paul Ford. "Overcoming steroid unresponsiveness in airways disease." Biochemical Society Transactions 37, no. 4 (July 22, 2009): 824–29. http://dx.doi.org/10.1042/bst0370824.

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Most of the patients with asthma are found to be successfully treated with conventional therapy. However, there are a small proportion of asthmatic patients who fail to respond to corticosteroids even at high doses or with supplementary therapy. In addition, even high doses of corticosteroids have a minimal effect on the inexorable decline in lung function in COPD (chronic obstructive pulmonary disease) and only a small effect in reducing exacerbations. Corticosteroid-insensitivity therefore presents a profound management problem. Corticosteroids act through a cytosolic receptor [GR (glucocorticoid receptor)], which is activated and translocates to the nucleus. Once in the nucleus, it either binds to DNA and switches on the expression of anti-inflammatory genes or represses the activity of distinct signalling pathways such as NF-κB (nuclear factor κB), AP-1 (activator protein-1) or MAPKs (mitogen-activated protein kinases). This latter step requires the recruitment of co-repressor molecules. A failure to respond to corticosteroids may therefore result from lack of binding to GR, reduced GR expression, lack of co-repressor activity or enhanced activation of inflammatory pathways. These events can be modulated by oxidative stress or high levels of inflammatory cytokines, which may lead to a reduced clinical outcome. Understanding the molecular mechanisms of GR action, and inaction, may lead to the development of new anti-inflammatory drugs or reverse the relative corticosteroid-insensitivity that is characteristic of these diseases.
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32

&NA;. "INDUCTION OF UNRESPONSIVENESS TO ORGAN ALLOGRAFTS." Transplantation 51, no. 4 (April 1991): 905–8. http://dx.doi.org/10.1097/00007890-199104000-00034.

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33

Venkataramaiah, Sudhir, Ganne S. Umamaheswara Rao, Sriganesh Kamath, Tanmay Jadhav, Channaveerachari Naveen Kumar, Shyam Sundar Arumugham, Madhusudan Reddy, Mariamma Philip, and Jagadisha Thirthalli. "Duration of Pupillary Unresponsiveness to Light." Journal of ECT 34, no. 4 (December 2018): e61-e64. http://dx.doi.org/10.1097/yct.0000000000000491.

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34

Propper, David, and Giuseppe Remuzzi. "Induction of unresponsiveness via intrathymic inoculation." Lancet 337, no. 8755 (June 1991): 1487–88. http://dx.doi.org/10.1016/0140-6736(91)93184-b.

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35

Remuzzi, Giuseppe, and Norberto Perico. "Induction of unresponsiveness via intrathymic inoculation." Lancet 338, no. 8764 (August 1991): 450. http://dx.doi.org/10.1016/0140-6736(91)91075-6.

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36

Freed, Simon. "Induced Specific Immunological Unresponsiveness & Conditioned Behavioral Reflexes, in Functional Isomorphism-Meditation and Conditioned Specific Unresponsiveness." International Journal of Neuroscience 44, no. 3-4 (January 1989): 275–81. http://dx.doi.org/10.3109/00207458908986207.

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37

Mueller, D. "Molecular mechanisms underlying functional T-cell unresponsiveness." Current Opinion in Immunology 7, no. 3 (1995): 375–81. http://dx.doi.org/10.1016/0952-7915(95)80113-8.

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38

Kawai, Taro, Osamu Adachi, Tomohiko Ogawa, Kiyoshi Takeda, and Shizuo Akira. "Unresponsiveness of MyD88-Deficient Mice to Endotoxin." Immunity 11, no. 1 (July 1999): 115–22. http://dx.doi.org/10.1016/s1074-7613(00)80086-2.

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39

Pence, Dena M., Angela R. Hague, Stacy K. Silvers, Richard L. Wasserman, Robert W. Sugerman, and Morley A. Herbert. "Sustained Unresponsiveness Following Food Oral Immunotherapy (FOIT)." Journal of Allergy and Clinical Immunology 139, no. 2 (February 2017): AB132. http://dx.doi.org/10.1016/j.jaci.2016.12.435.

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40

Ponzone, Alberto, Francesco Porta, Alessandro Mussa, Alessandra Alluto, Silvio Ferraris, and Marco Spada. "Unresponsiveness to tetrahydrobiopterin of phenylalanine hydroxylase deficiency." Metabolism 59, no. 5 (May 2010): 645–52. http://dx.doi.org/10.1016/j.metabol.2009.09.008.

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41

Wood, K. J. "Mechanisms of unresponsiveness to alloantigens in vivo." Transplantation Proceedings 30, no. 5 (August 1998): 2430–31. http://dx.doi.org/10.1016/s0041-1345(98)00675-7.

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42

G. T, Clark, and John C. Kelleher. "Specific unresponsiveness to skin allografts in burns." Plastic and Reconstructive Surgery 87, no. 6 (June 1991): 1154. http://dx.doi.org/10.1097/00006534-199106000-00072.

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43

Makari, George, William H. Hoffman, James E. Carroll, Diane R. Savage, and Theodora Van der Zalm. "Autonomic Dysfunction and Adrenocortical Unresponsiveness to ACTH." Journal of Child Neurology 3, no. 3 (July 1988): 174–76. http://dx.doi.org/10.1177/088307388800300304.

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44

Toste, Jessica R., Donald L. Compton, Douglas Fuchs, Lynn S. Fuchs, Jennifer K. Gilbert, Eunsoo Cho, Laura A. Barquero, and Bobette D. Bouton. "Understanding Unresponsiveness to Tier 2 Reading Intervention." Learning Disability Quarterly 37, no. 4 (January 17, 2014): 192–203. http://dx.doi.org/10.1177/0731948713518336.

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The purpose of the current study was to examine academic and cognitive profiles of first graders who responded adequately and inadequately to intensive small-group reading intervention (Tier 2), as well as assess how these profiles differ based on the criteria used for classification of unresponsiveness. Nonresponders were identified using two different methods: (a) reading composite with weighted standardized scores for untimed word identification and word attack, timed sight word reading and decoding, and reading comprehension at the end of first grade ( n = 23; 18.4%), and (b) local norms on first grade word identification fluency (WIF; n = 31; 24.8%). Repeated measures ANOVAs were used to assess the difference between responders and nonresponders on four separate profiles (i.e., academic and cognitive profiles, with groups identified using reading composite and WIF criteria for unresponsiveness). Significant level effects were found using the first-grade reading composite and the WIF criteria, indicating that the groups differ from one another across domains. Interestingly, there were only significant shape effects found when using the WIF criteria, suggesting relative strengths and weaknesses distinguish the groups. These findings suggest potentially important considerations related to identification and placement of students in appropriately intensive and targeted interventions.
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KOHYAMA, JUN, SEIICHI WATANABE, CHIKAO FUKUDA, KAZUHIKO SHIMOZAWA, and KIYOSHI SAITOH. "Adrenocorticotropic Hormone Unresponsiveness Associated with Hypertrophic Cardiomyopathy." Acta Paediatrica 78, no. 3 (May 1989): 482–87. http://dx.doi.org/10.1111/j.1651-2227.1989.tb11118.x.

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Bosson, D., N. Mees, J. Ranet, E. Vamos, F. Vertongen, and R. Wolter. "126 GENERALIZED MINERALOCORTICOID UNRESPONSIVENESS FAMILIAL RECESSIVE PSEUDOHYPOALDOSTERONISM." Pediatric Research 19, no. 6 (June 1985): 624. http://dx.doi.org/10.1203/00006450-198506000-00146.

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Hunt, G., C. Todd, and A. J. Thody. "Unresponsiveness of human epidermal melanocytes to MSH." Melanoma Research 5 (September 1995): 38. http://dx.doi.org/10.1097/00008390-199509001-00066.

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Kockler, Denise R., Michelle W. McCarthy, and Cathy L. Lawson. "Seizure Activity and Unresponsiveness after Hydroxycut Ingestion." Pharmacotherapy 21, no. 5 (May 2001): 647–51. http://dx.doi.org/10.1592/phco.21.6.647.34542.

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Payne, Donald N. R., Melissa Hubbard, and Sheila A. McKenzie. "Corticosteroid unresponsiveness in asthma: Primary or acquired?" Pediatric Pulmonology 25, no. 1 (January 1998): 59–61. http://dx.doi.org/10.1002/(sici)1099-0496(199801)25:1<59::aid-ppul7>3.0.co;2-j.

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Antonietta, La Terza, Papa Giampaolo, Miceli Cristina, Alimenti Claudio, and Luporini Pierangelo. "Unresponsiveness ofEuplotes focardiihsp70 genes to thermal stress." Italian Journal of Zoology 67, sup1 (January 2000): 111–14. http://dx.doi.org/10.1080/11250000009356364.

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