ABSTRACT
PURPOSE: To examine hospitalization as part of a complex pathway to care in first episode psychosis (FEP), exploring help-seeking episodes (HSE) and their relationship to hospitalization. METHODS: Data from 66 patients at the Early Psychosis Intervention Clinic New Orleans (EPIC-NOLA), a coordinated specialty care (CSC) clinic, was obtained from Pathways to Care (PTC) assessments, which documents elements of help seeking. A chart review was performed identifying hospitalizations. RESULTS: Most patients were hospitalized multiple times (n = 37, M = 2.98, SD = 2.14). On average, patients had more hospitalizations prior to starting treatment at EPIC-NOLA (M = 1.72, SD = 1.35) than after (M = 1.27, SD = 1.79). Patients whose first HSE resulted in intake at EPIC-NOLA were significantly less likely to be hospitalized after intake than patients with multiple HSE (F(1,52.3) = 12.9, p < .001). There was a significant correlation (N = 42) between HSE and hospitalizations after intake (τb = .327 p < .05); patients seeking help more often were more likely to be hospitalized after intake. No significant correlations were found between duration of untreated psychosis (DUP) and hospitalization. CONCLUSION: While results are correlational, several key relationships were noted. Fewer hospitalizations occurred after intake into EPIC-NOLA. Starting treatment after the first HSE was related to fewer future hospitalizations, compared to intake after multiple HSEs. Intake into a CSC clinic after a single HSE may reduce hospitalization. Additionally, increased HSE, not DUP, impacted patients' likelihood of hospitalization. This prompts treatment engagement during a first HSE to reduce hospitalization.
ABSTRACT
Ulcerative colitis (UC) causes chronic inflammation and damage to the colonic mucosal layer. Recent studies have reported significant changes in phosphatidylcholine (PC) and lysophosphatidylcholine (LPC) in UC patients and oral administration of PC has considerable therapeutic effects against UC, suggesting the metabolism of phosphatidylcholine may be involved in the UC development. Our previous work has demonstrated that berberine effectively suppresses inflammation and protects colonic mucosa injury in DSS-induced colitic mice. However, whether the therapeutic effects of berberine are attributed to its action on the PC metabolism remains unknown. In the present study, we have shown that berberine significantly reduces the lysophosphatidylcholine (LPC) levels in the sera of DSS-induced experimental colitis mice and LPS-stimulated macrophage RAW 264.7 cells. The cytosolic phospholipase A2a (PLA2G4A), an enzyme for hydrolyzing PC to LPC, was found to be up-regulated in the colon tissue of experimental colitis mice and inflamed macrophage RAW 264.7 cells. We then demonstrated berberine inhibits the phosphorylation of cytosolic phospholipase A2a (PLA2G4A) in the colon tissue of experimental colitis mice and inflamed macrophage RAW 264.7 cells. Subsequently, we revealed berberine suppressed the expression of pro-inflammatory factors including TNF-alpha and IL-6 through regulating PLA2G4A dysfunction in macrophage RAW 264.7 cells. Mechanistically, we found that berberine directly binds to PLA2G4A and inhibits MAPK/JNK signaling pathway to inhibit PLA2G4A activity in inflammatory status. Therefore, we concluded that berberine inhibits colonic PLA2G4A activity to ameliorate colonic inflammation in experimental colitic mice, suggesting modulation of the PC metabolism via PLA2G4A might be beneficial for establishing new therapies strategy for UC.
