Among various DNA computing algorithms, it is very common to create an initial data pool that covers correct and incorrect answers at first place followed by a series of selection process to destroy the incorrect ones. The surviving DNA sequences are read as the solutions to the problem. However, algorithms based on such a brute force search will be limited to the problem size. That is, as the number of parameters in the studied problem grows, eventually the algorithm becomes impossible owing to the tremendous initial data pool size. In this theoretical work, we modify a well-known sticker model to design an algorithm that does not require an initial data pool for SAT problem. We propose to build solution sequences in parts to satisfy one clause in a step, and eventually solve the whole Boolean formula after a number of steps. Accordingly, the size of data pool grows from one sort of molecule to the number of solution assignments. The proposed algorithm is expected to provide a solution to SAT problem and become practical as the problem size scales up.

Heat shock protein 70 (Hsp70) preconditioning induces thermotolerance, and adenosine monophosphate (AMP)‐activated protein kinase (AMPK) plays a role in the process of autophagy. Here, we investigated whether 17‐dimethylaminoethylamino‐17‐demethoxy‐geldanamycin (17‐DMAG) protected against heat stroke (HS) in rats by up‐regulation of Hsp70 and phosphorylated AMPK (pAMPK). To produce HS, male Sprague–Dawley rats were placed in a chamber with an ambient temperature of 42°C. Physiological function (mean arterial pressure, heart rate and core temperature), hepatic and intestinal injury, inflammatory mediators and levels of Hsp70, pAMPK and light chain 3 (LC3B) in hepatic tissue were measured in HS rats or/and rats pre‐treated with 17‐DMAG. 17‐DMAG pre‐treatment significantly attenuated hypotension and organ dysfunction induced by HS in rats. The survival time during HS was also prolonged by 17‐DMAG treatment. Hsp70 expression was increased, whereas pAMPK levels in the liver were significantly decreased in HS rats. Following pre‐treatment with 17‐DMAG, Hsp70 protein levels increased further, and pAMPK levels were enhanced. Treatment with an AMPK activator significantly increased the LC3BII/LC3BI ratio as a marker of autophagy in HS rats. Treatment with quercetin significantly suppressed Hsp70 and pAMPK levels and reduced the protective effects of 17‐DMAG in HS rats. Both of Hsp70 and AMPK are involved in the 17‐DMAG‐mediated protection against HS. 17‐DMAG may be a promising candidate drug in the clinical setting.

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In this paper, we study the routing problem for the undirected binary de Bruijn interconnection network. Researchers have never proposed a shortest path routing algorithm on the undirected binary de Bruijn network. We first propose a shortest path routing algorithm, whose time complexity in the binary de Bruijn network of 2 m m m nodes is O O O(m m m 2 ). Then, based on our shortest path routing algorithm, we propose two fault-tolerant routing schemes. It is assumed that at most one node fails in the network. In our schemes, two node-disjoint paths are found. Our first fault-tolerant routing algorithm guarantees that one of the two paths is the shortest path, and the other is of length at most m m m + log 2 m m m + 4. Our second algorithm can find two node-disjoint paths with lengths at most m m m and m m m + 4, respectively, if the shortest path is not required in the fault-tolerant routing.