This study suggests that periodontitis may be associated with an increased risk of PAD. This association could result from the increased concentration of serum inflammatory cytokines in those with periodontitis.

T. socranskii, T. denticola, and P. gingivalis were frequently detected in periodontitis patients by PCR. The prevalence of these 3 microorganisms was correlated with various clinical parameters. Taken together, our findings suggest that T. socranskii, T. denticola, and P. gingivalis are associated with the severity of periodontal tissue destruction.

This is the first study to identify oral microorganisms in the lesions of Buerger disease. Our findings suggest a possible etiologic link between Buerger disease and chronic infections such as oral bacterial infections.

5-Fluorouracil (5-FU) is a commonly used drug for the treatment of malignant cancers. However, approximately 80% of patients undergoing 5-FU treatment suffer from gastrointestinal mucositis. The aim of this report was to identify the drug target for the 5-FU-induced intestinal mucositis. 5-FU-induced intestinal mucositis was established by intraperitoneally administering mice with 100 mg/kg 5-FU. Network analysis of gene expression profile and bioluminescent imaging were applied to identify the critical molecule associated with 5-FU-induced mucositis. Our data showed that 5-FU induced inflammation in the small intestine, characterized by the increased intestinal wall thickness and crypt length, the decreased villus height, and the increased myeloperoxidase activity in tissues and proinflammatory cytokine production in sera. Network analysis of 5-FU-affected genes by transcriptomic tool showed that the expression of genes was regulated by nuclear factor-κB (NF-κB), and NF-κB was the central molecule in the 5-FU-regulated biological network. NF-κB activity was activated by 5-FU in the intestine, which was judged by in vivo bioluminescence imaging and immunohistochemical staining. However, 5-aminosalicylic acid (5-ASA) inhibited 5-FU-induced NF-κB activation and proinflammatory cytokine production. Moreover, 5-FU-induced histological changes were improved by 5-ASA. In conclusion, our findings suggested that NF-κB was the critical molecule associated with the pathogenesis of 5-FU-induced mucositis, and inhibition of NF-κB activity ameliorated the mucosal damage caused by 5-FU.

T. forsythensis, C. rectus, P. gingivalis, and T. denticola were the predominant periodontopathic bacteria of aggressive periodontitis patients in Japan. Although A. actinomycetem- comitans was also detected in AgP patients, the prevalence of this bacterium was much lower than that of P. gingivalis.

Periodontopathic bacteria were present in a high percentage of specimens of diseased arteries from AAA patients and were found throughout the whole aneurysmal wall. These bacteria may play a role in the development of AAAs and/or contribute to weakening the aneurysmal wall.

Long-term memory requires activity-dependent synthesis of plasticity-related proteins (PRPs) to strengthen synaptic efficacy and consequently consolidate memory. Cytoplasmic polyadenylation element binding protein (CPEB)3 is a sequence-specific RNA-binding protein that regulates translation of several PRP RNAs in neurons. To understand whether CPEB3 plays a part in learning and memory, we generated CPEB3 knock-out (KO) mice and found that the null mice exhibited enhanced hippocampus-dependent, short-term fear memory in the contextual fear conditioning test and long-term spatial memory in the Morris water maze. The basal synaptic transmission of Schaffer collateral-CA1 neurons was normal but long-term depression evoked by paired-pulse low-frequency stimulation was modestly facilitated in the juvenile KO mice. Molecular and cellular characterizations revealed several molecules in regulating plasticity of glutamatergic synapses are translationally elevated in the CPEB3 KO neurons, including the scaffolding protein PSD95 and the NMDA receptors along with the known CPEB3 target, GluA1. Together, CPEB3 functions as a negative regulator to confine the strength of glutamatergic synapses by downregulating the expression of multiple PRPs and plays a role underlying certain forms of hippocampusdependent memories.

Melt crystallization of racemic polylactide (equimolar PLLA/PDLA) blend upon slow cooling (1 °C/min from 270 °C) was studied via a combination of wide-angle X-ray scattering (WAXS), differential scanning calorimetry (DSC), and Fourier-transform infrared spectroscopy (FTIR). Results indicated extensive development of racemic (32/31) helical pairs below 220 °C, followed by emergence of a broad mesomorphic peak in the WAXS profile below 190 °C; the intensity of this mesophase peak started to decrease at 150 °C, with concomitant emergence of WAXS- or DSC-discernible formation of stereocomplex (βc) crystals. Isothermal measurements at 200 vs 170 °C revealed the presence of low vs high populations of helical pairs; βc crystals were observed to develop only at 170 °C but not at 200 °C, indicating the need for adequate population of racemic helical pairs for formation of their mesomorphic clusters in the melt matrix as precursors of βc nuclei. The clear change in the melt structure well before the formation of incipient βc crystals reflects strong driving force under large supercooling toward transformation, but the transformation process is kinetically suppressed: only after extensive development of racemic helices and emergence of mesomorphic clusters in the melt matrix may nucleation occur. These observations suggest that the nucleation process proceeds in elementary units of preformed helical pairs in the melt matrix, with an intermediate stage of clustered helical pairs before incipience of βc crystals.