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Randomized trial of an electronic asthma monitoring system among New York City children

Jacobson, Judith S; Lieblein, Andrea; Fierman, Arthur H; Fishkin, Edward R; Hutchinson, Vincent E; Rodriguez, Luis; Serebrisky, Denise; Chau, Michelle; Saperstein, Arnold
OBJECTIVES: To test the efficacy of an electronic asthma monitoring system (AMS) to reduce pediatric emergency department (ED) visits and hospitalizations for asthma. STUDY DESIGN: Randomized clinical trial. METHODS: Families of pediatric patients with asthma aged 8 to 17 years were recruited at 6 medical centers. Children were randomly assigned to the American Medical Alert Corporation pediatric AMS or a paper diary. The numbers of and costs associated with ED visits and hospitalizations for the 2 groups in the year following randomization were compared using t tests of statistical significance. RESULTS: Of 59 children recruited to the trial, 29 were randomized to the AMS and 30 to the diary. The 2 groups were similar in demographic and clinical characteristics. During their study year, 24 AMS group members logged on a mean (SD) of 211.0 (117.3) days; 13 diary group members provided data on a mean (SD) of 136.6 (128.0) days. During the 32 months that the study was in progress, the case managers logged on a mean (SD) of 171.0 (97.2) days. Overall, 35 children had at least 1 ED visit, but only 7 children were hospitalized. The 2 groups had no statistically significant differences in the numbers of or charges associated with ED visits or hospitalizations. CONCLUSION: Electronic devices are being developed to make chronic disease management easier for patients and their families, but they should not be adopted without careful study, including randomized trials, to ascertain their use, costs, and benefits
PMID: 19895185
ISSN: 1936-2692
CID: 141664

ADRENALECTOMY FAILS TO ABOLISH CORTICOTROPIN-RELEASING FACTOR (CRF)-INDUCED IMMUNOSUPPRESSION IN HUMANS AS WELL AS RATS [Meeting Abstract]

NABRISKI, D; SHAPIRO, M; SAPERSTEIN, A; SHENKMAN, L; VALENTINE, FT; YAO, JS; ROSENZWEIG, S; HUTCHINSON, B; AUDYHA, T; HOLLANDER, CS
ISI:A1992HN74101352
ISSN: 0009-9279
CID: 52005

LONG-TERM THYROXINE THERAPY DOES NOT AFFECT BONE-MINERAL DENSITY IN PREMENOPAUSAL WOMEN [Meeting Abstract]

NABRISKI, D; SHAPIRO, M; SAPERSTEIN, A; ERAS, C; LIDOR, J; SHENKMAN, L; AUDHYA, T; HOLLANDER, CS
ISI:A1992HN74101353
ISSN: 0009-9279
CID: 52006

Interleukin 1 beta mediates stress-induced immunosuppression via corticotropin-releasing factor

Saperstein A; Brand H; Audhya T; Nabriski D; Hutchinson B; Rosenzweig S; Hollander CS
Intracerebroventricular (icv) infusion of human interleukin 1 beta (IL-1) into intact and adrenalectomized rats impairs immune function. Using antibody to IL-1 as well as an inhibitor of IL-1 action, we sought to determine if endogenous IL-1 in the central nervous system has a physiological role in mediating the immunosuppressive effects of stress. Compared with freely moving controls, rats given intermittent electric shock to the tail for 40 min exhibited a fall in T lymphocyte proliferation and natural killer (NK) cell cytotoxicity of 33% and 38%, respectively; however, when pretreated with icv human IL-1 monoclonal antibody, which significantly crossreacts with rat IL-1, the decrement was attenuated to 14.6% and 15%, respectively. When rats were pretreated with icv alpha-MSH, which blocks many IL-1 effects, shock-induced suppression of 42% in both T lymphocyte proliferation and NK cytotoxicity were blunted to 33% and 31%, respectively. Similar results were found in adrenalectomized rats. These findings suggest that endogenous IL-1 is a physiologically relevant mediator of the immune response to stress. As IL-1 has been reported to release CRF, which we have shown always plays a significant role in stress-induced immunomodulation, we then assessed the relationship of IL-1 and CRF in immunosuppression. Infusion of icv IL-1 caused a decrease of 35% in T lymphocyte proliferation and 34% in NK activity, but pretreatment with CRF antibody icv attenuated IL-1 suppression of T lymphocyte proliferation and NK activity to 10% and 8%, respectively. Comparable results were observed in adrenalectomized rats. These findings suggest that CRF antibody is able to block the immunosuppressive effects of IL-1. To further examine the interaction of CRF in mediating stress-induced immunosuppression, we found that animals pretreated with icv CRF antibody, shocked and then given icv IL-1, had a decrement in T lymphocyte proliferation and NK cytotoxicity of 24% and 21%, respectively, demonstrating that the immunosuppressive effect of icv IL-1 is blocked when central CRF has been neutralized by prior administration of icv CRF antibody. In contrast, animals pretreated with icv IL-1 antibody, shocked and then given icv CRF, had decrements of 38% and 40%, respectively, showing that icv CRF does act even when central IL-1 has been neutralized by prior administration of icv IL-1 antibody. Thus, we conclude there is a sequential relationship between two of the known mediators of stress-induced immunosuppression, with release of central IL-1 followed by that of CRF
PMID: 1309324
ISSN: 0013-7227
CID: 13802

SEQUENTIAL RELEASE OF INTERLEUKIN 1-BETA AND CORTICOTROPIN-RELEASING FACTOR MEDIATES STRESS-INDUCED IMMUNOSUPPRESSION [Meeting Abstract]

SAPERSTEIN, A; NABRISKI, D; BRAND, H; ROSENZWEIG, S; HUTCHINSON, B; HOLLANDER, CS; AUDHYA, T
ISI:A1991FH32301035
ISSN: 0009-9279
CID: 51617

CRF-INDUCED IMMUNOSUPPRESSION INVIVO IS MEDIATED AT A CENTRAL LOCUS, IRRESPECTIVE OF ITS ROUTE OF ADMINISTRATION [Meeting Abstract]

NABRISKI, D; SAPERSTEIN, A; HUTCHINSON, B; ROSENZWEIG, S; AUDHYA, T; HOLLANDER, CS
ISI:A1991FH32301037
ISSN: 0009-9279
CID: 51618

CORTICOTROPIN-RELEASING FACTOR SUPPRESSES INTERLEUKIN-2 INDUCED LYMPHOCYTE-PROLIFERATION AND INCREASES CAMP PRODUCTION IN HUMAN SPLENOCYTES [Meeting Abstract]

AUDHYA, T; NABRISKI, D; SAPERSTEIN, A; RANSON, J; HOLLANDER, CS
ISI:A1991FH32301825
ISSN: 0009-9279
CID: 51621

CENTRAL INTERLEUKIN 1-BETA INDUCES IMMUNOSUPPRESSION BY STIMULATING CENTRAL CRF MESSENGER-RNA AND CRF RELEASE [Meeting Abstract]

SAPERSTEIN, A; NABRISKI, D; BRAND, H; HUTCHINSON, B; ROSENZWEIG, S; AUDHYA, T; HOLLANDER, CS
ISI:A1991FH32301863
ISSN: 0009-9279
CID: 51622

Corticotropin-releasing factor modulates the immune response to stress in the rat

Jain R; Zwickler D; Hollander CS; Brand H; Saperstein A; Hutchinson B; Brown C; Audhya T
We examined the role of CRF, a key mediator of the endocrine response to stress, in modulating immunosuppression during the subacute stress of intermittent electrical shock over 1 h. Administration of shock to intact rats resulted in a 74% decrement in T-lymphocyte proliferation and a 59% decrease in natural killer cytotoxicity. Similar suppression of these two parameters of immune function in response to shock was noted in adrenalectomized rats as well. The immunosuppressive effects of this shock were significantly and comparably blunted when both intact and adrenalectomized animals were pretreated 1) iv with either a highly potent polyclonal CRF antibody or a specific CRF antagonist or 2) intracerebroventricularly with either a high affinity monoclonal antibody to CRF or a specific CRF antagonist. An immunomodulatory role for CRF is further supported by the findings that administration of exogenous CRF, either iv (10 micrograms/animal) or intracerebroventricularly (1 microgram/animal), resulted in significant decrements in lymphocyte proliferation and natural killer cytotoxicity, similar to those seen with the stress paradigm. Our observations indicate that CRF plays a significant role in modulating the immune response to subacute stress, largely by adrenal-independent mechanisms
PMID: 1999154
ISSN: 0013-7227
CID: 14115

Role of corticotropin-releasing factor in immunosuppression

Nabriski D; Saperstein A; Brand H; Jain R; Zwickler D; Hutchinson B; Rosenzweig S; Hollander CS; Audhya T
PMID: 1668987
ISSN: 0066-9458
CID: 14233