Facial emotion recognition and alexithymia in Chinese male patients with deficit schizophrenia.

Deficit schizophrenia (DS) has been proposed as a pathophysiologically distinct schizophrenia subtype. This study investigated facial emotion recognition deficits and alexithymia in DS and non-deficit schizophrenia patients (NDS) and their relationships with other clinical variables. The Brief Psychiatric Rating Scale (BPRS), Scale for the Assessment of Negative Symptoms (SANS), and Scale for the Assessment of Positive Symptoms (SAPS) were employed to evaluate the psychiatric symptoms in patients with schizophrenia. Facial emotion recognition deficits and Alexithymia were assessed in DS, NDS, and control groups by The Chinese Facial Emotion Test (CFET) and the Toronto Alexithymia Scale-20 (TAS-20). Compared with control group, both DS and NDS patients exhibited more severe facial emotion recognition impairments, with the exception of "happy faces" in NDS patients, as well as higher alexithymia scores. In DS patients, correct frequency for fear recognition and total CFET score were negatively correlated with TAS-20 Factor 3 subscore for "externally oriented thinking". Total TAS-20 score was positively correlated with BPRS negative symptom and SANS score in DS patients. In contrast, there were no correlations between TAS-20 scores/subscores and psychiatric symptoms in NDS patients. These findings indicated distinct facial emotion recognition impairments in DS and NDS patients. Alexithymia might be specifically related to the negative symptom in DS patients, suggesting DS as a unique schizophrenic subtype.

[Effect of glucagon-like peptide-1 on hypoxia-reoxygenation induced injury in neonatal rat cardiomyocytes].

OBJECTIVE: To observe the effect of glucagon-like peptide-1 (GLP-1) on hypoxia-reoxygenation (H/R) induced injury in neonatal rat cardiomyocytes. METHODS: Cultured neonatal rat cardiomyocytes were randomly divided into seven groups: normal control group, H/R group, GLP-1 + H/R group, GLP-1 + H/R + UO126 group, GLP-1 + H/R + LY294002 group, H/R + UO126 group, H/R + LY294002 group. LDH activity, apoptosis rate of cardiomyocytes, Caspase-3 activity were detected. RESULTS: Compared with normal control group, the activity of LDH, cardiomyocyte apoptosis rate, Caspase-3 activity were all significantly increased in H/R group (all P < 0.01). However, compared with H/R group, these changes were significantly attenuated in GLP-1 + H/R group [the activity of LDH (128.47 +/- 7.96) U/L vs. (223.96 +/- 22.10) U/L, P < 0.01, and cardiomyocyte apoptosis rate (2.84 +/- 2.56)% vs. (12.58 +/- 6.69)%, P < 0.01, and Caspase-3 activity (36,809 +/- 4750) RLU vs. (57,602 +/- 9161) RLU, P < 0.01], while LY294002 (PI3K inhibitor) and UO126 (MAPK inhibitor) could block the effects of GLP-1 in cardiomyocytes underwent H/R injury. CONCLUSIONS: GLP-1 could protect H/R injury mainly by inhibiting cardiomyocytes apoptosis via activating PI3K/Akt and MAPK signaling pathway.

Effects and mechanism of glucagon-like peptide-1 on injury of rats cardiomyocytes induced by hypoxia-reoxygenation.

BACKGROUND: Although the insulinotropic role of glucagon-like peptide-1 (GLP-1) in type 2 diabetes mellitus has been substantiated, its role in cardioprotection remains largely unknown. This study aimed to determine the effects of GLP-1 on injury of rats cardiac myocytes induced by hypoxia-reoxygenation (H/R) and the possible mechanisms. METHODS: The cultured neonatal rats cardiac myocytes were randomly divided into seven groups: the normal control group, the H/R group, the GLP-1 + H/R group, the GLP-1 + H/R + UO126 (the p42/44 mitogen-activated protein kinase (MAPK) inhibitor) group, the GLP-1 + H/R + LY294002 (phosphatidylinositol 3-kinase (PI3K) inhibitor) group, the H/R + UO126 group, and the H/R + LY294002 group. The lactate dehydrogenase (LDH) activity, apoptosis rate of cardiac myocytes, and caspase-3 activity were detected after the injury of H/R. RESULTS: Compared with the normal control group, the activity of LDH, cardiac myocyte apoptosis rate, and caspase-3 activity all increased significantly in the H/R group (P < 0.01). Compared with the H/R group, these three indices all decreased in the H/R + GLP-1 group (P < 0.01). However, the changes of LDH activity, apoptosis rate, and caspase-3 activity were inhibited by LY294002 and UO126 respectively. CONCLUSIONS: GLP-1 can directly act on cardiac myocytes and protect them from H/R injury mainly by inhibiting their apoptosis. Its mechanism may be through the PI3K-Akt pathway and the MAPK signaling pathway.

[Effects of injection of Huangqi injectio into Zusanli (ST 36) on immune function in the patient of schizophrenia].

OBJECTIVE: To study on effects of injection of Huangqi Injectio into Zusanli (ST 36) on the hospital infection and immune function in the patient of schizophrenia. METHODS: Thirty inpatients of chronic schizophrenia were treated with injection of Huangqi Injectio into bilateral Zusanli (ST 36), 2 mL each point, thrice each week, for 8 weeks. Relative immune indexes and the hospital infection were investigated. RESULTS: The hospital infection and the sub-infection were 4 cases (13.3%), 7 cases-times (23.3%) in the injection group; and 9 cases (15.0%), 19 cases-times (31.7%) in the control group, respectively, with no significant difference between the two groups (P>0.05). The drug-administration duration was 7.77 days/case and 11.87 days/case in the two groups, respectively (P<0.01). In the injection group, as compared with that of last 3 years the duration was 7.77 days/case and 14.08 days/case (P<0.01). IgG, IgA, IgM and T-cell subgroups did not have significant changes, but there was the most different value before and after injection in SIL-2R of the no-infection group, and the longer the drug administration duration, the smaller the different values. CONCLUSION: Injection of Huangqi Injectio into Zusanli (ST 36) has definite effect for prevention of the hospital infection in inpatients of chronic schizophrenia, and SIL-2R is a valuable index for investigation of the hospital of infection.