In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Several studies suggest that the open reading frame 3 (ORF3) gene of porcine epidemic diarrhea virus (PEDV) is related to viral infectivity and pathogenicity, but its function remains unknown. Here, we propose a structure model of the ORF3 protein consisting of four TM domains and forming a tetrameric assembly. ORF3 protein can be detected in PEDV-infected cells and it functions as an ion channel in both Xenopus laevis oocytes and yeast. Mutation analysis showed that Tyr170 in TM4 is important for potassium channel activity. Furthermore, viral production is reduced in infected Vero cells when ORF3 gene is silenced by siRNA. Interestingly, the ORF3 gene from an attenuated PEDV encodes a truncated protein with 49 nucleotide deletions, which lacks the ion channel activity.
PEDV ORF3 encodes an ion channel protein and regulates virus production

Aims: The chronic consumption of alcohol is known to result in neurodegeneration and impairment of cognitive function. Pathological and neuroimaging studies have confirmed that brain atrophy in alcoholics is mainly due to widespread white matter (WM) loss with neuronal loss restricted to specific regions, such as the prefrontal cortex. Neuroimaging studies of cigarette smokers also suggest that chronic inhalation of tobacco smoke leads to brain atrophy, although the neurotoxic component is unknown. As a high proportion of chronic alcoholics also smoke cigarettes it has been hypothesized that at least some alcohol-related brain damage is due to tobacco smoke exposure. Methods: 39 Long Evans rats were subjected to 8 weeks exposure to alcohol and/or 5 weeks coexposure to nicotine-specific nitrosamine ketone (NNK), a proxy for tobacco smoke. Their frontal WM was then assayed with transmission electron microscopy. Results: NNK and ethanol co-exposure had a synergistic effect in decreasing myelinated fibre density. Furthermore, NNK treatment led to a greater reduction in myelin sheath thickness than ethanol whereas only the ethanol-treated animals showed a decrease in unmyelinated fibre density. Conclusion: These data suggest that NNK causes WM degeneration, an effect that is exacerbated by alcohol, but unlike alcohol, it has little impact on the neuronal components of the brain.
The Differential Effects of Alcohol and Nicotine- Specific Nitrosamine Ketone on White Matter Ultrastructure

Last year marked the 40th anniversary of the publication of the first print edition of Mendelian Inheritance in Man (MIM). 1 This seems an appropriate juncture at which to review its origins, evolution, and present status, including and particularly those of its online version, OMIM (Online Mendelian Inheritance in Man). This is an opportunity, at the same time, to review in brief the rapid progress in an important part of medical genetics and genomics, as chronicled in MIM/OMIM over these 40 years, and to contemplate the future challenges of OMIM. MIM 1,2 is a comprehensive knowledgebase of human genes and genetic disorders. It consists of full-text overviews of genes and genetic phenotypes, particularly disorders, and is useful to students, researchers, and clinicians. It was initiated in the early 1960s as a trilogy of catalogs of autosomal dominant, autosomal recessive, and X-linked phenotypes. It has been maintained as an electronic file since 1964 and has been published in 12 print editions ( fig. 1) , the first in 1966, the most recent (in three volumes) in 1998. (Various editions of MIM were translated into Russian [1976], Spanish [1976], and Mandarin [1996]; see fig. 2.) In

PERSPECTIVES IN HUMAN GENETICS Mendelian Inheritance in Man and Its Online Version, OMIM Origins and Evolution of the Structure and Organization and Content of MIM/OMIM