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Background: Excess nutrients induce adipose inflammation. Results: Excess glucose and palmitate generate ROS via NOX4 by a mechanism that involves the PPP and translocation of NOX4 into LRs, rather than by mitochondrial oxidation. Conclusion: NOX4 activates monocyte chemotactic factor expression. Significance: Understanding the source of ROS generation may lead to the development of new therapeutic targets for adipose tissue inflammation.

Gingival fibroblasts produce proinflammatory cytokines in response to lipopolysaccharide (LPS) from periodontopathic bacteria. Recently it has become evident that the human homologue of Drosophila Toll can transduce intracellular signaling by LPS stimulation. Toll-like receptors (TLRs) have been identified in myeloid cells; however, their role in nonmyeloid cells such as gingival fibroblasts has not been fully elucidated. Here, we report that human gingival fibroblasts constitutively express TLR2 and TLR4 and that their levels of expression are increased by stimulation with LPS from Porphyromonas gingivalis. Upregulated expression of interleukin-6 gene and protein in fibroblasts stimulated with LPS is inhibited by anti-TLR4 antibody. These findings suggest that TLRs may confer responsiveness to LPS in gingival fibroblasts.

Rationale Macrophage accumulation in adipose tissue associates with insulin resistance and increased cardiovascular disease risk. We previously have shown that generation of reactive oxygen species (ROS) and monocyte chemotactic factors after exposure of adipocytes to saturated fatty acids (SFAs) such as palmitate occurs via translocation of NADPH oxidase 4 (NOX4) into lipid rafts (LRs). The anti-inflammatory effects of apolipoprotein A-I (apoA-I) and HDL on macrophages and endothelial cells appears to occur via cholesterol depletion of LRs. However, little is known concerning anti-inflammatory effects of HDL and apoA-I on adipocytes. Objective To determine whether apoA-I and HDL inhibit inflammation in adipocytes and adipose tissue, and whether this is dependent on LRs. Methods and Results In 3T3L-1 adipocytes, apoA-I, HDL and methyl-β-cyclodextrin inhibited chemotactic factor expression. ApoA-I and HDL also disrupted LRs, reduced plasma membrane cholesterol content, inhibited NOX4 translocation into LRs, and reduced palmitate-induced ROS generation and monocyte chemotactic factor expression. Silencing ABCA-1 abrogated the effect of apoA-I, but not HDL, while silencing ABCG-1 or SRB-1 abrogated the effect of HDL but not apoA-I. In vivo, apoA-I transgenic mice fed a high fat, high sucrose, cholesterol-containing diet showed reduced chemotactic factor and pro-inflammatory cytokine expression and reduced macrophage accumulation in adipose tissue. Conclusion ApoA-I and HDL have anti-inflammatory effects in adipocytes and adipose tissue similar to their effects in other cell types. These effects are consistent with disruption and removal of cholesterol from LRs, which are regulated by cholesterol transporters such as ABCA-1, ABCG-1 and SRB-1.

The effects of Porphyromonas gingivalis lipopolysaccharide (P-LPS) and Escherichia coli lipopolysaccharide (E-LPS) on the gene expression and production of inflammatory cytokines of human periodontal ligament fibroblasts (HPLF) were examined by a Northern (RNA blot) assay and enzyme-linked immunosorbent assay, respectively. mRNAs for interleukin-6 (IL-6), IL-8, and transforming growth factor beta (TGF-␤) were detected in HPLF cells, but IL-1␣, IL-1␤, tumor necrosis factor alpha, transforming growth factor alpha, and granulocyte-macrophage colony-stimulating factor were not detected by reverse transcription-PCR. The expression of TGF-␤ mRNA was not influenced by either LPS. P-LPS (1 to 10 g/ml) and E-LPS (100 g/ml) markedly stimulated the expression of IL-6 and IL-8 mRNAs compared with the control. The synthesis of IL-6 and IL-8 was also stimulated by 10 and 100 g of both LPSs per ml, but IL-8 synthesis was not stimulated with E-LPS at 1 g/ml. Secretion of IL-6 and IL-8 into the culture medium was detected at 6 and 3 h, respectively, after exposure to P-LPS (10 g/ml). These findings suggested that P. gingivalis leads to periodontal tissue destruction and alveolar bone resorption through IL-6 and IL-8 released from HPLF cells stimulated with its LPS.

Ultrasound elastography is a relatively new diagnostic technique for measuring the elasticity (hardness) of tissue. Eleven years have passed since the debut of elastography. Various elastography devices are currently being marketed by manufacturers under different names. Pancreatic elastography can be used not only with transabdominal ultrasonography but also with endoscopic ultrasonography, but some types of elastography are difficult to perform for the pancreas. These guidelines aim to classify the various types of elastography into two major categories depending on the differences in the physical quantity (strain, shear wave), and to present the evidence for pancreatic elastography and how to use pancreatic elastography in the present day. But the number of reports on ultrasound elastography for the pancreas is still small, and there are no reports on some elastography devices for the pancreas. Therefore, these guidelines do not recommend methods of imaging and analysis by elastography device.

Patients with abdominal aortic aneurysm appear to have an approximately 3-fold increased risk for both inguinal and postoperative incision hernia compared to patients with aortoiliac occlusive disease. A large multi-centre prospective study is needed to confirm the results of this review.

Although fimbriae of Porphyromonas gingivalis have been implicated as playing a major role in adherence to gingival tissue surfaces, no conclusive genetic evidence has yet been obtained. ThefimA gene, the determinant for the major fimbrial subunit protein, was cloned and sequenced (D.