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ObjectiveTo investigate the social support status and influencing factors of schizophrenics in remission in Northeast Sichuan， and to provide ideas for improving their social support.MethodsFrom May to September 2020， a total of 533 patients who met the diagnosis criteria of the International Classification of Diseases， tenth edition （ICD-10） for schizophrenics in remission at the mental health institutions in Guangyuan， Bazhong and Dazhou cities were selected for the survey， and patients were assessed by self-made demographic and clinical data inventory and Social Support Rating Scale （SSRS）. Then the social support status of schizophrenic in remission and influencing factors were analyzed， meantime， the impact of the second round reimbursement policy of medical insurance benefits on their social support was addressed particularly.Results①The SSRS total score， objective support， subjective support， and utilization of support scores of schizophrenics in remission were lower than those of the national norm （t=5.065~30.382， P5 000 yuan （F=15.892）， patient's economic income （t=4.083）， and outpatient or online follow-up （F=3.954）， with statistically significant differences （P

β654-thalassemia is a prominent Chinese subtype of b-thalassemia, representing 17% of all cases of β-thalassemia in China. The molecular mechanism underlying this subtype involves the IVS-2-654 C→T mutation leading to aberrant β-globin RNA splicing. This results in an additional 73-nucleotide exon between exons 2 and 3 and leads to a severe thalassemia syndrome. Herein, we explored a CRISPR/Cas9 genome editing approach to eliminate the additional 73- nucleotide by targeting both the IVS-2-654 C→T and a cryptic acceptor splice site at IVS-2-579 in order to correct aberrant b-globin RNA splicing and ameliorate the clinical β-thalassemia syndrome in β654 mice. Gene-edited mice were generated by microinjection of sgRNA and Cas9 mRNA into one-cell embryos of β654 or control mice: 83.3% of live-born mice were gene-edited, 70% of which produced correctly spliced RNA. No off-target events were observed. The clinical symptoms, including hematologic parameters and tissue pathology of all of the edited β654 founders and their offspring were significantly improved compared to those of the non-edited β654 mice, consistent with the restoration of wild-type b-globin RNA expression. Notably, the survival rate of gene-edited heterozygous β654 mice increased significantly, and liveborn homozygous β654 mice were observed. Our study demonstrated a new and effective gene-editing approach that may provide groundwork for the exploration of β654-thalassemia therapy in the future.