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1.
Psychosomatics ; 60(3): 263-270, 2019.
Article in English | MEDLINE | ID: mdl-30166118

ABSTRACT

BACKGROUND: Previous studies have demonstrated that proactive psychiatric consultation reduces hospital length of stay (LOS) in the general medical setting; however this model has not been studied in the intensive care unit (ICU). OBJECTIVE: To compare outcomes between a conventional consultation model and a proactive psychiatric consultation model. METHODS: Two medical ICUs (MICUs) were randomized to proactive psychiatric consultation vs conventional consultation psychiatric models. Proactive consultation included embedding a psychiatrist into daily MICU team rounds on all patients. In the conventional consultation MICU, psychiatric consultations were activated when deemed necessary. Primary outcomes were hospital LOS and MICU LOS. Secondary outcomes included delirium-coma-free hours and ventilator-free hours. RESULTS: A total of 429 patients were admitted to the proactive consultation MICU; 393 patients were admitted to the conventional consultation MICU. The consultation rate for the intervention group was 24.2% vs 6.1% in the control group (p < 0.001). Time to psychiatric consultation was shorter in the intervention group. Median hospital LOS was 6.92 days, interquartile range 3.70-14.31 in the intervention group vs 7.69 days, interquartile range 3.95-16.21 in the control group (p = 0.113). MICU LOS, delirium-coma-free hours, and ventilator-free hours were not significantly different between the 2 groups. Among the respiratory failure subgroup, hospital LOS was shorter in the intervention vs control group (median 9.46 days, interquartile range 4.95-17.56 vs 12.29 days, interquartile range 6.58-21.10, p = 0.011). CONCLUSIONS: Proactive psychiatric consultation in a MICU was associated with decreased time to consultation among all patients and shorter hospital LOS among patients with respiratory failure.


Subject(s)
Intensive Care Units/organization & administration , Length of Stay/statistics & numerical data , Mental Disorders/diagnosis , Referral and Consultation/organization & administration , Delirium/diagnosis , Delirium/therapy , Female , Humans , Intensive Care Units/statistics & numerical data , Male , Mental Disorders/therapy , Middle Aged , Prospective Studies , Referral and Consultation/statistics & numerical data , Respiratory Insufficiency/psychology , Respiratory Insufficiency/therapy
3.
Cell ; 128(5): 853-64, 2007 Mar 09.
Article in English | MEDLINE | ID: mdl-17350573

ABSTRACT

UV-induced pigmentation (suntanning) requires induction of alpha-melanocyte-stimulating hormone (alpha-MSH) secretion by keratinocytes. alpha-MSH and other bioactive peptides are cleavage products of pro-opiomelanocortin (POMC). Here we provide biochemical and genetic evidence demonstrating that UV induction of POMC/MSH in skin is directly controlled by p53. Whereas p53 potently stimulates the POMC promoter in response to UV, the absence of p53, as in knockout mice, is associated with absence of the UV-tanning response. The same pathway produces beta-endorphin, another POMC derivative, which potentially contributes to sun-seeking behaviors. Furthermore, several instances of UV-independent pathologic pigmentation are shown to involve p53 "mimicking" the tanning response. p53 thus functions as a sensor/effector for UV pigmentation, which is a nearly constant environmental exposure. Moreover, this pathway is activated in numerous conditions of pathologic pigmentation and thus mimics the tanning response.


Subject(s)
Genes, p53 , Hyperpigmentation/metabolism , Skin Pigmentation , Skin/metabolism , Transcriptional Activation , Ultraviolet Rays/adverse effects , Animals , Apoptosis , Carcinoma, Basal Cell/genetics , Carcinoma, Basal Cell/metabolism , Cell Culture Techniques , Cell Line, Tumor , Foreskin/metabolism , Foreskin/pathology , Humans , Keratinocytes/cytology , Keratinocytes/metabolism , Keratinocytes/radiation effects , Male , Melanocytes/metabolism , Melanocytes/radiation effects , Mice , Mice, Inbred C57BL , Mice, Knockout , Pro-Opiomelanocortin/genetics , Promoter Regions, Genetic , RNA, Messenger/genetics , RNA, Messenger/metabolism , Skin/radiation effects , Skin Neoplasms/genetics , Skin Neoplasms/metabolism , Tumor Suppressor Protein p53/metabolism , Up-Regulation , alpha-MSH/metabolism , beta-Endorphin/metabolism
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