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Miyauchi S, Maekawa T, Aoki Y, Miyazawa H, Tabeta K, Nakajima T, Yamazaki K. Oral infection with Porphyromonas gingivalis and systemic cytokine profile in C57BL/6.KOR-ApoEshl mice. J Periodont Res 2012; 47: 402-408. © 2011 John Wiley & Sons A/S Background and Objective: Periodontal infection affects atherosclerotic diseases, such as coronary heart diseases. Mouse models have revealed that oral infection with Porphyromonas gingivalis induces changes in inflammatory- and lipid metabolism-related gene expression, regardless of the development of atherosclerotic lesions. However, the serum protein expression profile in the oral infection model has not been investigated. The present study aimed to analyse the effect of oral infection with P. gingivalis on the expression levels of multiple cytokines in the serum in apolipoprotein E-deficient mice by using a cytokine antibody array. Material and Methods: C57BL/6.KOR- Apoe shl mice were orally infected with P. gingivalis five times at 3 day intervals and were then killed. Splenocytes were isolated and analysed for proliferative activity and immunoglobulin G (IgG) production in response to in vitro restimulation with P. gingivalis. The expression levels of various cytokines in the sera were analysed using a mouse antibody array glass chip. Results: Splenocytes from P. gingivalis-infected mice demonstrated significantly greater proliferation and IgG production in response to P. gingivalis compared with those from sham-infected mice. Antibody array analysis revealed the selective upregulation of matrix metalloproteinase 3, intercellular adhesion molecule 1, insulin-like growth factor binding protein 2 and chemokine (C-X-C motif) ligand 7 and the downregulation of interleukin-17, tumor necrosis factor-α and L-selectin. Conclusion: These data demonstrate that oral infection with P. gingivalis induces alterations in systemic cytokine production. These cytokines could play roles in the development not only of periodontitis but also of atherosclerosis. [ABSTRACT FROM AUTHOR]

NaS2 is a Na+-coupled transporter for sulfate that belongs to the SLC13 gene family. This transporter was originally cloned from high endothelial venule endothelial cells, but nothing is known about the functional characteristics of this transporter except that it transports sulfate in a Na+-coupled manner. Northern blot analysis indicates that NaS2 is expressed most robustly in placenta. In the present study, we cloned NaS2 from rat placenta and characterized its transport function in detail using the Xenopus laevis oocyte expression system. Rat NaS2 consists of 629 amino acids and is highly similar to human NaS2. In situ hybridization studies with mouse placental sections show that NaS2 transcripts are expressed primarily in trophoblasts of the labyrinth zone. The expression of the transporter is confirmed in primary cultures of trophoblasts isolated from human placenta. When expressed in X. laevis oocytes, rat NaS2 mediates Na+-coupled transport of sulfate. The transport of sulfate is inhibited by oxyanions of selenium, chromium, arsenic, molybdenum, and phosphorous, suggesting that the transporter may mediate the transport of these oxyanions in addition to sulfate. The Kt for sulfate is 153±30μM and the Na+:sulfate stoichiometry is 3:1. The transport process is electrogenic as evidenced from the inhibition of the uptake process by K+-induced depolarization. We conclude that NaS2 is a placenta-specific Na+-coupled, electrogenic, transporter for sulfate expressed in trophoblasts and that it is also responsible for the transport of oxyanions of the micronutrients selenium and chromium. [Copyright &y& Elsevier]

We present a patient whose ectopic calcification following deep posterior compartment syndrome was studied by electron microscopy, chemical analyses, and X-ray diffraction. The patient complained of a toe flexion deformity following a tibial fracture which he sustained 18 years earlier. Damage to the peroneal artery was demonstrated by magnetic resonance angiography, suggesting that the patient had had deep posterior compartment syndrome in the past. A large radiopaque mass, identified in the flexor hallucis longus muscle by radiographs and computed tomography, was resected, resulting in a dramatic improvement of the toe deformity. The resected material was analyzed in detail. It included no osseous tissue, and was not birefringent under a polarizing microscope, being compatible with ectopic calcification rather than ossification. On electron microscopy the material was found to be an assembly of tiny rods. Chemical and X-ray diffraction analyses suggested a carbonate-containing apatite as the most probable substance. [ABSTRACT FROM AUTHOR]

The concentration and molecular weight of hyaluronan (HA) in the synovial fluid of the hip joint were determined in 13 patients (aged 62.8 +/- 9.4 years) who had undergone prior total hip arthroplasty(THA), 23 patients (aged 65.0 +/- 8.2 years) with osteoarthritis of the hip joint (OA), and 13 patients (aged 40.2 +/- 2.7 years) with idiopathic osteonecrosis of the femoral head (ION). A sample of synovial fluid was obtained during revision THA because of loosening of the total hip prosthesis for the THA group, and during the first replacement surgery or osteotomy for the OA and ION groups. The concentration of HA in the synovial fluid was 0.64 +/- 0.42 mg/ml in the THA group, 1.07 +/- 0.28 mg/ml in the OA group, and 1.30 +/- 0.56 mg/ml in the ION group. The concentration of HA in the synovial fluid of the THA patients was significantly lower than that of the OA and ION patients (P = 0.0156 vs OA, P = 0.003 vs ION). The molecular weight of HA was 309 +/- 88.3 x 10(4) Da in the THA group, 377 +/- 201 x 10(4) Da in the OA group, and 240 +/- 148 x 10(4) Da in the ION group; these values do not differ significantly (P = 0.259 vs OA, P = 0.174 vs ION). Among the THA patients, there was no relation between the concentration of HA and the age of the patient, length of time since the first operation, or type of prosthesis fixation; there was also no relation between the molecular weight of HA and each of these factors. These results suggest that a pseudosynovial membrane is regenerated after THA, and that it produces HA of the same molecular weight as that in patients with OA and ION, although in smaller quantities. [ABSTRACT FROM AUTHOR]

Objective: This study was undertaken to investigate changes in chondroitin sulfate levels in the cervix and the physiologic role of chondroitin sulfate isomers in the process of cervical ripening.Study Design: Uterine cervical mucus samples were obtained from 57 women (7 nonpregnant women, 19 at preterm gestation, 9 at term gestation, 16 during the first stage of term labor, and 6 with threatened premature labor). Chondroitin sulfate isomer (chondroitin 0-sulfate, 4-sulfate, and 6-sulfate) concentrations in cervical mucus were measured by high-performance liquid chromatography. The effect of exogenous chondroitin sulfate on hyaluronidase activity in cervical mucus was evaluated by gel permeation chromatography of fluorolabeled hyaluronic acid.Results: Chondroitin sulfate concentrations in cervical mucus were increased significantly (P <. 05) in the threatened premature labor group compared with the preterm and term groups. However, the same finding was not observed in the first stage of term labor. Exogenous chondroitin sulfate inhibited hyaluronidase activity in mucus.Conclusion: Chondroitin sulfate may defend against cervical ripening in threatened premature labor. [ABSTRACT FROM AUTHOR]