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Introduction Involuntary admissions are increasing in numbers across Europe.1 They can be traumatic for the patients2 and are associated with large societal costs.3 Individuals with psychotic disorder are at particularly elevated risk of involuntary admission. Objectives This study aims to investigate whether machine learning methods including natural language processing can predict involuntary admission among patients with psychotic disorder. Methods We have obtained a dataset based on electronic health records for all patients having had at least one contact with the psychiatric services in the Central Denmark Region from 2011 to 2021. This dataset covers more than 120,000 patients, of which approximately 10,000 have been diagnosed with a psychotic disorder. The dataset contains both structured data, such as diagnoses, blood tests etc., as well as unstructured data (text). We will train machine learning models, basic logistic regression-models as well as state-of-the-art neural networks, to predict involuntary admission after contacts to the psychiatric services. Results As the machine learning models are under development, no results are available at this time. Preliminary results are expected in spring 2022. Conclusions If involuntary admission can be predicted among patients with psychotic disorder based on data from electronic health records, it will pave the way for potentially preventive interventions. References: 1. Sheridans-Rains, L et al., 2019 2. Frueh, B.C et al., 2005 3. Smith,S., 2020 Disclosure No significant relationships.

Background: Genetic immunization is expected to induce the expression of antigens in a native form. The encoded peptide epitopes are presented on endogenous MHC molecules, mimicking antigen presentation during a viral infection. We have explored the potential of enfuvirtide (T20), a short HIV peptide with antiviral properties, to enhance immune response to HIV antigens. To generate an expression vector, the T20 sequence was cloned into a conventional plasmid, the novel minicircle construct, and a replicon plasmid. In addition, 3 conventional plasmids that express the envelope of HIV-1 subtypes A, B and C and contain T20 in their gp41 sequences were also tested. Results: All combinations induced HIV-specific antibodies and cellular responses. The addition of T20 as a peptide and as an expression cassette in the 3 DNA vectors enhanced antibody responses. The highest anti-HIV-1 Env titers were obtained by the replicon T20 construct. This demonstrates that besides its known antiviral activity, T20 promotes immune responses. We also confirm that the combination of slightly divergent antigens improves immune responses. Conclusions: The antiretroviral T20 HIV-1 sequence can be used as an immunogen to elicit binding and neutralizing antibodies against HIV-1. These, or similarly modified gp41 genes/peptides, can be used as priming or boosting components for induction of broadly neutralizing anti-HIV antibodies. Future comparative studies will reveal the optimal mode of T20 administration.

Background Juvenile‐onset spinocerebellar ataxia has been recognized in Jack Russell Terriers and related Russell group terriers (RGTs) for over 40 years. Ataxia occurs with varying combinations of myokymia, seizures, and other signs of neurologic disease. More than 1 form of the disease has been suspected. Hypothesis/Objectives The objective was to identify the mutation causing the spinocerebellar ataxia associated with myokymia, seizures, or both and distinguish the phenotype from other ataxias in the RGTs. Animals DNA samples from 16 RGTs with spinocerebellar ataxia beginning from 2 to 12 months of age, 640 control RGTs, and 383 dogs from 144 other breeds along with the medical records of affected dogs were studied. Methods This case‐control study compared the frequencies of a KCNJ10 allele in RGTs with spinocerebellar ataxia versus control RGTs. This allele was identified in a whole‐genome sequence of a single RGT with spinocerebellar ataxia and myokymia by comparison to whole‐genome sequences from 81 other canids that were normal or had other diseases. Results A missense mutation in the gene coding for the inwardly rectifying potassium channel Kir4.1 (KCNJ10:c.627C>G) was significantly (P