High-resolution CT findings in Streptococcus milleri pulmonary infection.

AIM: To assess pulmonary high-resolution computed tomography (CT) findings in patients with acute Streptococcus milleri pulmonary infection. MATERIALS AND METHODS: Sixty consecutive patients with acute S. milleri pneumonia who had undergone high-resolution CT chest examinations between January 2004 and March 2010 were retrospectively identified. Twenty-seven patients with concurrent infections were excluded. The final study group comprised 33 patients (25 men, 8 women; aged 20-88 years, mean 63.1 years) with S. milleri infection. The patients' clinical findings were assessed. Parenchymal abnormalities, enlarged lymph nodes, and pleural effusion were evaluated on high-resolution CT. RESULTS: Underlying conditions included malignancy (n = 15), a smoking habit (n = 11), and diabetes mellitus (n = 8). CT images of all patients showed abnormal findings, including ground-glass opacity (n = 24), bronchial wall thickening (n = 23), consolidation (n = 17), and cavities (n = 7). Pleural effusion was found in 18 patients, and complex pleural effusions were found in seven patients. CONCLUSION: Pulmonary infection caused by S. milleri was observed mostly in male patients with underlying conditions such as malignancy or a smoking habit. The CT findings in patients with S. milleri consisted mainly of ground-glass opacity, bronchial wall thickening, pleural effusions, and cavities.

A clinical feature of hyperlipidemia in patients with central diabetes insipidus.

In this study, we analyzed plasma lipid and lipoprotein levels before and after treatment with 1-desamino-8-D-arginine vasopressin (DDAVP) in subjects with partial and complete central diabetes insipidus (DI) in order to determine how a shortage and supplement of this hormone affect plasma lipid metabolism. The subjects consisted of 6 patients with partial and 6 with complete central DI. After treatment with DDAVP through nasal cavity, plasma total cholesterol (TC) level did not decrease either in complete or partial form. Plasma triglyceride (TG) levels decreased from 306+/-175 mg/dl to 198+/-91 (35% decrease, p=0.027) in complete form, while TG did not change significantly in partial form. A detailed investigation of plasma lipoprotein metabolism during treatment with DDAVP was carried out in 3 of the 6 subjects with complete form of DI. Lipoprotein lipase activity and mass in post-heparin plasma from those three subjects tended to increase after treatment with DDAVP, along with the complete disappearance of an unusual lipoprotein between low density lipoprotein (LDL) and very low density lipoprotein (VLDL) as analyzed by polyacrylamide gel electrophoresis. These results suggest that the DDAVP treatment has a favorable effect on lipid and lipoprotein metabolism, especially triglyceride-rich lipoproteins, either directly or through modifying factors contributing to lipid metabolism.

Effect of troglitazone on plasma lipid metabolism and lipoprotein lipase.

AIMS: To clarify how troglitazone, an insulin-sensitizing agent, affects lipid metabolism and postheparin plasma lipoprotein lipase (LPL). METHODS: Fifteen patients (3 male, 12 female) (the average age 62+/-7 years; the mean body mass index (BMI) 25+/-3 kg/m2 ) were recruited for this study. The serum lipids and postheparin plasma lipoprotein lipase (LPL) mass before and 4 weeks after oral administration of troglitazone (200 mg day-1 ) were measured. A mouse preadipocyte cell line, 3T3-L1, was incubated with troglitazone and LPL enzyme protein mass in the culture media was measured by an enzyme linked immunosorbent assay. A reverse transcription polymerase chain reaction (RT-PCR) using primers specific for the carboxyl terminal 135 amino acid of mouse LPL cDNA was used to evaluate the effect of troglitazone on expression of LPL and Northern blot analysis carried out to determine expression of LPL. RESULTS: The average levels before treatment of fasting serum total cholesterol, triglycerides, high density lipoprotein cholesterol, plasma glucose and glycohaemoglobin A1c were 5.6+/-0.9, 1.8+/-1.0, 1.5+/-0.5, 8.1+/-1.7 mmol l-1 and 7.8+/-1.6% respectively. Four weeks after treatment, those levels were 5.4+/-0.9, 1.2+/-0.3 (P=0.004), 1.6+/-0.5 (P=0.02) mmol l-1, 7.7+/-2.3 mmol l-1 and 7. 3+/-0.6% (P=0.01), respectively. The postheparin plasma LPL mass increased from 226+/-39 to 257+/-68 ng ml-1 (P=0.03) during that period. The LPL mass in the media of 3T3 L1 cells cultured in the presence of 10, 20 or 30 microm of this compound increased in a dose dependent manner. RT-PCR revealed that the area of the bands of the RT-PCR products on 1.5% agarose gel analyzed with NIH image from the cell extracts cultured in the presence of 10 microm troglitazone was significantly larger (P=0.0069) than that in the absence of this compound. Northern blot analysis revealed that in the cultured 3T3-L1 cells, the expression of LPL was enhanced in the presence of 10 microm troglitazone. CONCLUSIONS: Troglitazone improves plasma triglyceride-rich lipoproteins metabolism by enhancing the expression of LPL in adipocytes.

Serotonin (5-hydroxytryptamine, 5-HT) enhances migration of rat aortic smooth muscle cells through 5-HT2 receptors.

The effects of serotonin on migration of cultured rat aortic smooth muscle cells (SMC) were studied to clarify the role of this substance in the pathogenesis of atherosclerosis. Serotonin alone did not stimulate SMC migration but stimulated it at physiological concentrations in the presence of other migration factors such as SMC-derived migration factor, platelet-derived migration factor and fibronectin. Checker-board analysis revealed that the serotonin effect was chemotactic. Moreover, serotonin effects were completely abolished by a selective inhibitor of the 5-HT2 receptor (MCI-9042), indicating that serotonin effects were mediated through the 5-HT2 receptor pathway. Finally, serotonin effects were also abolished by a phospholipase C inhibitor, U73122, suggesting that the 5-HT2 receptor mediated signal of serotonin was transduced by PLC. The results suggest that platelet-derived serotonin plays some role in the SMC dominant neointima formation.

Role of phospholipase A2 in expression of the scavenger pathway in cultured aortic smooth muscle cells stimulated with phorbol 12-myristate 13-acetate.

We have demonstrated that cultured intimal smooth muscle cells (SMC) from thickened intima can metabolize acetylated low-density lipoprotein (LDL) by a scavenger pathway, but medial SMC from normal arteries cannot. In this study we investigated the expression mechanism of the scavenger pathway in medial SMC using a phorbol ester. Medial SMC were incubated with 10(-10)-10(-7) M phorbol 12-myristate 13-acetate (PMA) for 1-24 h and then their degradation of 125I-labelled acetylated LDL was assayed. Unstimulated SMC degraded little acetylated LDL, but incubation for 24 h with PMA dose-dependently stimulated its degradation by SMC, the optimal PMA concentration being 1 x 10(-8) M. Induction of expression of the scavenger pathway required more than 4 h of incubation with PMA and was completely inhibited by cycloheximide. In addition expression of the scavenger pathway was not transient but stable. Induction of expression of the scavenger pathway by PMA was not inhibited by protein kinase C inhibitors, but was inhibited about 50% by phospholipase A2 inhibitors. The study, using various phorbol esters, indicated that induction of the scavenger pathway was well correlated with their ability to stimulate phospholipase A2 in medial SMC but not with their ability to activate protein kinase C. Moreover, incubation with exogenous phospholipase A2 (0.1-10 units/ml) or its product, lysophosphatidylcholine (0.01-100 micrograms/ml) dose-dependently increased degradation of 125I-labelled acetylated LDL in medial SMC. Lysophosphatidylcholine was most effective in various lysophospholipids. These results suggest that PMA induced the scavenger pathway in part by stimulating phospholipase A2 in medial SMC, and that a product, lysophosphatidylcholine, is a mediator of expression of the scavenger pathway.

Platelet-derived growth factor is a potent stimulator of expression of intercellular adhesion molecule-1 in human arterial smooth muscle cells.

The effects of platelet-derived growth factor (PDGF) on the expression of intercellular adhesion molecule-1 (ICAM-1) as an indicator of cell activation were investigated in cultured human arterial smooth muscle cells (SMC). PDGF-BB and -AB but not -AA at 2-10 ng/ml stimulated ICAM-1 expression at a subconfluent but not a confluent state in a dose-dependent manner. ICAM-1 expression was induced at 2h, reached a plateau at 4h, and continued for at least 24h after stimulation with PDGF. The maximal stimulatory effect of PDGF-BB at 10 ng/ml was comparable to that by optimal concentrations of other cytokines and inflammatory agents. These data suggested that PDGF was a potent stimulator of ICAM-1.