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The objective of our research is to create efficient methods and tools for the quick and thorough assessment of emerging digital circuit devices, facilitating the adoption of promising ones. In this work, we develop methods and tools for hybrid technology that combines memristors with MOS transistors and demonstrates their effectiveness. Although several types of memristor-transistor logic have been proposed, 15 years of research has created a small set of logic cells. We propose a systematic method for generating new and efficient memristor-transistor single-phase combinational logic cells. At the core of our approach is a cell enumerator, which enables us to explore a wide range of cell designs, including nonintuitive ones, and a data-driven inductive learning method, which identifies new properties of such cells and scales up our explorations. In conjunction with other completely new tools, these create a comprehensive and definitive library of logic cells. Our new cells provide significant improvements or significantly distinct Pareto-optimal alternatives for the few logic functions for which prior research has created cells. Importantly, our methods enable us to discover a previously unknown synergistic operation between memristors and transistors that occurs for specific cell topologies. We harness this synergy to develop a method for adding memristors to low-area pass-transistor circuits such that they produce strong output voltages and low power, including for patterns that cause ratioed operation. We have also developed a new memristor-transistor logic family, namely controlled-AND (cAND)/controlled-OR (cOR), which includes many of the best cells. We have also developed a constructive method for designing such cells. 

C. difficile infection (CDI) is a costly and increasing burden on the healthcare systems of many 11 developed countries due to the high rates of nosocomial infections. Despite the availability of 12 several antibiotics with high response rates, effective treatment is hampered by recurrent 13 infections. One potential mechanism for recurrence is the existence of C. difficile biofilms in the 14 gut which persist through the course of antibiotics. In this review, we describe current 15 developments in understanding the molecular mechanisms by which C. difficile biofilms form 16 and are stabilized through extracellular biomolecular interactions. 

ABSTRACT Mucins are glycoproteins which can be found in host cell membranes and as a gelatinous surface formed from secreted mucins. Mucosal surfaces in mammals form a barrier to invasive microbes, particularly bacteria, but are a point of attachment for others.Clostridioides difficileis an anaerobic bacterium, which colonizes the mammalian gastrointestinal (GI) tract and is a common cause of acute GI inflammation leading to a variety of negative outcomes. AlthoughC. difficiletoxicity stems from secreted toxins, colonization is a prerequisite forC. difficiledisease. WhileC. difficileis known to associate with the mucous layer and underlying epithelium, the mechanisms underlying these interactions that facilitate colonization are less well understood. To understand the molecular mechanisms by whichC. difficileinteracts with mucins, we usedex vivomucosal surfaces to test the ability ofC. difficileto bind to mucins from different mammalian tissues. We found significant differences inC. difficileadhesion based upon the source of mucins, with highest levels of binding observed to mucins purified from the human colonic adenocarcinoma line LS174T and lowest levels of binding to porcine gastric mucin. We also observed defects in adhesion by mutants deficient in flagella but not type IV pili. These results imply that interactions between host mucins andC. difficileflagella facilitate the initial host attachment ofC. difficileto host cells and secreted mucus. IMPORTANCEClostridioides difficileis one of the leading causes of hospital-acquired infections worldwide and presents challenges in treatment due to recurrent gastrointestinal disease after treatment with antimicrobials. The mechanisms by whichC. difficilecolonizes the gut represent a key gap in knowledge, including its association with host cells and mucosa. Our results show the importance of flagellin for specific adhesion to mucosal hydrogels and can help to explain prior observations of adhesive defects in flagellin and pilin mutants.