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              <text>As the adoption of Large Language Models (LLMs) is becoming ubiquitous, understanding their pitfalls is becoming increasingly urgent. LLMs are known to hallucinate and may be subject to cascading hallucinatory generations due to their autoregressive structure and exposure bias. This paper first introduces the topic of hallucination cascade, covering relevant literature. Then an experiment is presented on the propagation of hallucination through long answer text generation, for all combinations of five LLMs - Qwen2 (0.5B), Qwen2 (7B), Llama3.1 (8B), Gemma2 (9B) and Mistral-NeMo (12B) - at five levels of temperature: 0, 0.75, 1, 1.25, 2. In a novel methodology, responses are generated by the five LLMs, then labelled by two more LLMs as hallucinatory or not on both a token and sentence level. The labelling is done with clear instructions and additional context to ensure its quality. Correlational evidence was found on both granularity levels that hallucinatory tokens are positively autocorrelated at lag 1, and that autocorrelation monotonically decreases as lag increases (token level only), supporting the cascading hallucination hypothesis. Finally, some hallucination mitigating techniques are presented, with both research and application in mind. All the code used for the empirical part of this paper (Section 3) can be found at https://github.com/LucMekouar/URSS_2024.</text>
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              <text>The membranes of the mammalian cell are host to many membrane-bound transcription regulators which need to be collocated to the nucleus to act on both inter and extracellular processes ​(1)​ . For our project we chose to focus on the membrane of the endoplasmic reticulum, which research has shown to be a region where proteins (or peptide fragments) are able to cycle between the ER and the nucleus in order to influence gene transcription.​(2)​ The pseudoproteases iRhom (of the rhomboid super family) ​(3)​ have been identified as such proteins with a distinct function related to their cleavage from the ER and subsequent nuclear transport. This cleavage is conducted via the Signal Peptidase Complex (SPC) which cleaves either side of the first transmembrane domain, resulting in an N terminal fragment. This fragment is then transported to the nucleus where it can affect gene expression. This process has been shown to be elevated in pathologies such as psoriasis and oesophageal cancer. ​(4)​   Our goal was to investigate if other proteins (TMEM214, TRPV4, TOR4A) with regions similar to iRhom cleavage sites undergo the same SPC cleavage mechanism. Evidence of cleavage would suggest the proteins could possess a similar transcription regulation function, potentially linking to other pathologies.</text>
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