Repetitive transcranial magnetic stimulation combined with olanzapine and amisulpride for treatment-refractory schizophrenia.

BACKGROUND: Treatment-refractory schizophrenia (TRS), accounting for approximately 30% of all schizophrenia cases, has poor treatment response and prognosis despite treatment with antipsychotic drugs. AIM: To analyze the therapeutic effectiveness of repetitive transcranial magnetic stimulation (rTMS) combined with olanzapine (OLZ) and amisulpride (AMI) for TRS and its influence on the patient's cognitive function. METHODS: This study enrolled 114 TRS patients who received treatment at the First Affiliated Hospital of Zhengzhou University between July 2019 and July 2022. In addition to the basic OLZ + AMI therapy, 54 cases of the control group (Con group) received modified electroconvulsive therapy, while 60 cases of the research group (Res group) received rTMS. Data on therapeutic effectiveness, safety (incidence of drowsiness, headache, nausea, vomiting, or memory impairment), Positive and Negative Symptom Scale, Montreal Cognitive Assessment Scale, and Schizophrenia Quality of Life Scale were collected from both cohorts for comparative analyses. RESULTS: The Res group elicited a higher overall response rate and better safety profile when compared with the Con group. Additionally, a significant reduction was observed in the post-treatment Positive and Negative Symptom Scale and Schizophrenia Quality of Life Scale scores of the Res group, presenting lower scores than those of the Con group. Furthermore, a significant increase in the Montreal Cognitive Assessment Scale score was reported in the Res group, with higher scores than those of the Con group. CONCLUSION: The treatment of TRS with rTMS and OLZ + AMI is effective and safe. Moreover, it can alleviate the patients' mental symptoms, improve their cognitive function and quality of life, and has a high clinical application value.

Development of a Novel Tear Lipid Test Strip.

PURPOSE: The unifying characteristic of dry eye is the loss of tear film homeostasis, and the tear lipid layer is a key component for maintaining film stability. The detection of tear lipid is of great significance for the diagnosis of dry eye. In this study, we explored a new test strip for the detection of tear lipid. METHODS: The tear lipid test strip was prepared by coating the strip material with hydrophobic nano-silica. We tested its physical properties with iodine vapor chromogenic and cobalt chloride test methods. Its biosafety was evaluated by an ocular irritation test in rabbits. Finally, we established a rabbit meibomian gland dysfunction model and measured both eyes with the tear lipid test strip at the first, third, seventh, 14th, 16th, and 21st day after surgery. RESULTS: The tear lipid test strip had fine lipophilicity and hydrophobicity. It can extract lipid from tear, and the tear lipid can be quantified by measuring the length of lipid infiltration. In the ocular irritation test, the test strip had no obvious eye irritation. The length of lipid infiltration between experimental and control rabbit eyes began to show statistical difference since the third day after surgery. CONCLUSIONS: The novel tear lipid test strip has great lipophilicity, hydrophobicity, and biological safety. It might be effectively applied in diagnosis of dry eye.

Knockdown of HIPK2 attenuates the pro-fibrogenic response of hepatic stellate cells induced by TGF-ß1.

Homeodomain-interacting protein kinase 2 (HIPK2), a member of HIPKs family, is considered as a key regulator in fibrosis. However, the roles of HIPK2 in hepatic stellate cells (HSCs) activation and liver fibrosis are still unclear. Therefore, in this study, we investigated the roles of HIPK2 in HSCs activation and liver fibrosis. Our results showed that HIPK2 expression was significantly up-regulated in liver fibrotic tissues and TGF-ß1-treated HSCs. Knockdown of HIPK2 significantly inhibited TGF-ß1-induced HSCs proliferation, as well as decreased the expression levels of α-SMA and collagen I. Furthermore, knockdown of HIPK2 attenuated the phosphorylation of Smad3 in the presence of TGF-ß1. In conclusion, these results demonstrated that HIPK2 may function as a novel regulator to modulate HSC activation, potentially by inhibiting the TGF-ß1/Smad3 signaling pathway. The results provide supporting evidence that HIPK2 may be a potential target for the treatment of liver fibrosis.