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A four-membered square-shaped H-bonding structure was successfully designed to synthesize vitamin D3 co-crystals. The co-crystallization process was found to be conformationally selective to result in topochemically stable materials.

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BackgroundThe distribution of the Chinese Glyptosternoid catfish is limited to the rivers of the Tibetan Plateau and peripheral regions, especially the drainage areas of southeastern Tibet. Therefore, Glyptosternoid fishes are ideal for reconstructing the geological history of the southeastern Tibet drainage patterns and mitochondrial genetic adaptions to high elevations.ResultsOur phylogenetic results support the monophyly of the Sisoridae and the Glyptosternoid fishes. The reconstructed ancestral geographical distribution suggests that the ancestral Glyptosternoids was widely distributed throughout the Brahmaputra drainage in the eastern Himalayas and Tibetan area during the Late Miocene (c. 5.5 Ma). We found that the Glyptosternoid fishes lineage had a higher ratio of nonsynonymous to synonymous substitutions than those found in non-Glyptosternoids. In addition, ωpss was estimated to be 10.73, which is significantly higher than 1 (p-value 0.0002), in COX1, which indicates positive selection in the common ancestral branch of Glyptosternoid fishes in China. We also found other signatures of positive selection in the branch of specialized species. These results imply mitochondrial genetic adaptation to high elevations in the Glyptosternoids.ConclusionsWe reconstructed a possible scenario for the southeastern Tibetan drainage patterns based on the adaptive geographical distribution of the Chinese Glyptosternoids in this drainage. The Glyptosternoids may have experienced accelerated evolutionary rates in mitochondrial genes that were driven by positive selection to better adapt to the high-elevation environment of the Tibetan Plateau.Electronic supplementary materialThe online version of this article (doi:10.1186/s12862-015-0516-9) contains supplementary material, which is available to authorized users.

As the global market for fisheries and aquaculture products expands, mislabeling of these products has become a growing concern in the food safety arena. Molecular species identification techniques hold the potential for rapid, accurate assessment of proper labeling. Here we developed and evaluated DNA barcodes for use in differentiating United States domestic and imported catfish species. First, we sequenced 651 base-pair barcodes from the cytochrome oxidase I (COI) gene from individuals of 9 species (and an Ictalurid hybrid) of domestic and imported catfish in accordance with standard DNA barcoding protocols. These included domestic Ictalurid catfish, and representative imported species from the families of Clariidae and Pangasiidae. Alignment of individual sequences from within a given species revealed highly consistent barcodes (98% similarity on average). These alignments allowed the development and analyses of consensus barcode sequences for each species and comparison with limited sequences in public databases (GenBank and Barcode of Life Data Systems). Validation tests carried out in blinded studies and with commercially purchased catfish samples (both frozen and fresh) revealed the reliability of DNA barcoding for differentiating between these catfish species. The developed protocols and consensus barcodes are valuable resources as increasing market and governmental scrutiny is placed on catfish and other fisheries and aquaculture products labeling in the United States.

Four cocrystals of the anti-tuberculosis drug pyrazinamide (PZA) with adipic acid (1), sebacic acid (2), trans-aconitic acid (3), and citric acid (4) were successfully designed and synthesised. Their structures were determined by single-crystal X-ray diffraction, in which 1 and 2 displayed one-dimensional chain structures, while 3 and 4 formed two-dimensional hydrogen bonded frameworks between PZA and the coformers. The equilibrium solubility and intrinsic dissolution rate (IDR) of the four cocrystals and PZA itself were then determined. The results demonstrate that 3 and 4 exhibit superior solubility and IDR relative to PZA.

Accumulating evidence suggested that neuroinflammation played a crucial role in dopaminergic neuronal death in Parkinson's disease (PD). The receptor for advanced glycation end products (RAGE), a multi-ligand receptor of the immunoglobulin superfamily, has been proposed as a key molecule in the onset and sustainment of the inflammatory response. Engagement of RAGE contributed to neuroinflammation by upregulating nuclear factor-κB (NF-κB) as well as cytokines. The aim of the present study was to investigate the expression of RAGE in 1-methyl-4-phenyl-1,2,3,6tetrahydropyridine (MPTP)-treated mice and elucidate the RAGE signal pathway involved in the inflammation. Results showed that RAGE protein and pro-inflammatory cytokines cyclooxygenase type 2 (COX-2) were upregulated in MPTP-treated mice. Further experiments showed that RAGE ablation inhibited phosphorylation of IκB and p38 and protected nigral dopaminergic neurons against cell death in the substantia nigra (SN). These results suggested that RAGE participated in the pathogenesis of PD by neuroinflammation and p38MAPK-NFκB signal pathway may be involved in the process. Moreover, interfering with RAGE signaling pathway may be a reasonable therapeutic option in slowing PD development and progression.

Thymosin beta4 is a major actin-sequestering molecule. Here, we report a prominent upregulation of thymosin beta4 in the hippocampus following entorhinal deafferentation. Northern blotting displayed a transient increase of thymosin beta4 mRNA in the deafferented hippocampus by 1.8, 2.3, 1.3 and 1.1-fold of controls, respectively, at 1, 3, 7 and 15 days post-lesion. In-situ hybridization confirmed that the induction of thymosin beta4 mRNA specifically occurred in the entorhinally denervated zones of the hippocampus. The double labeling of in-situ hybridization for thymosin beta4 mRNA with isolectin B4 cytochemistry showed that isolectin B4-positive microglial cells are responsible for deafferentation-induced thymosin beta4 mRNA expression. The results suggest that thymosin beta4 may participate in the process of microglial activation, which is the earliest event in lesion-induced plasticity.