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The type 1 fimbriae of uropathogenic Escherichia coli (UPEC) have been described as important for the establishment of bladder infections and urinary tract infections (UTI). Urinary prostaglandin (PG) levels and cyclooxygenase (COX)-2 expression in urine particulates may increase with infectious and inflammatory processes, including UTIs. We investigated the mechanisms underlying the modulation of COX-2 expression through the invasion of type 1 fimbriated UPEC strain J96 (J96-1) in human bladder 5637 cells. Bladder 5637 cells infected with J96-1 induced increases in the expression of COX-2 and secretion of PGE(2) . By using specific inhibitors and short hairpin RNA (shRNA), we have demonstrated that the activation of extracellular signal-related kinase (ERK), c-Jun-NH(2) -terminal kinase (JNK) and p38 MAPK pathways is critical for J96-1-induced COX-2 expression. Luciferase reporters and chromatin immunoprecipitation assays suggest that J96-1 invasion increases NF-κB- and AP-1-DNA-binding activities in 5637 cells. Inhibition of NF-κB and AP-1 activations blocked the J96-1-induced COX-2 promoter activity and expression. The effect of J96-1 on 5637 cell signalling and COX-2 expression is mediated by Toll-like receptor (TLR)-4. In summary, our findings provide the molecular pathways underlying type 1 fimbriated J96-dependent COX-2 expression in 5637 cells, providing insight into the function of UPEC invasion in bladder epithelial cells.

A rapid, simple, and nonradioactive method for diagnosing point mutations of c-K-ras oncogenes in gastroenterologic cancers is described. This method involved the selective amplification of DNA fragments from cancer tissues of surgical specimens with specific oligonucleotide primers, followed by digestion with restriction enzymes that recognized artificially created or naturally occurring restriction sites. To detect codon 12 mutations, an artificial Msp I site was created by introducing a single nucleotide mismatch into the 5' mutagenesis primer. Using a similar approach, an Hae III site was created to detect codon 13 mutations. Bal I and MBo II sites were used to detect codon 61 mutations. A total of 61 gastroenterologic cancer cases were studied. Of 35 cases of colorectal cancer, 7 showed mutations: 6 at codon 12 and 1 at codon 13. In 1 of 2 cases of cholangiocellular carcinoma, point mutation at codon 12 was found. One case of duodenal cancer showed point mutation at codon 12. No mutations were found in the cases of hepatocellular carcinoma (4), gastric cancer (12), esophageal cancer (3), or pancreatic cancer (2).

Incorporation of active devices/media such as transistors for microwave and gain media for optics may be very attractive for enabling desired low loss and broadband metamaterials. Such metamaterials can even have gain which may very well lead to new and exciting physical phenomena. We investigate microwave composite right/left-handed transmission lines (CRLH-TL) incorporating ideal gain devices such as constant negative resistance. With realistic lumped element values, we have shown that the negative phase constant of this kind of transmission lines is maintained (i.e., left-handedness kept) while gain can be obtained (negative attenuation constant of transmission line) simultaneously. Possible implementation and challenging issues of the proposed active CRLH-TL are also discussed.

Chronic inflammation is a well-recognized complication in dialysis patients and a potential role of the adipose tissue as an important tissue of origin contributing to inflammation has been proposed. Stable peritoneal dialysis (PD) patients were enrolled to investigate the relationship between serum levels of proinflammatory cytokines and adipokines. Our results revealed that there was a strong association between high sensitivity C-reactive protein and interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-alpha) but not with IL-10 and IL-18. IL-6 correlated with TNF-alpha, IL-10, and IL-18. No association was found between IL-10 and IL-18. Adiponectin was positively correlated with all proinflammatory cytokines, except IL-10. No significant association was found between resistin and proinflammatory cytokines. Hepatocyte growth factor (HGF) was directly related to proinflammatory cytokines but not with adipokines. The presence of residual kidney function (RKF) affected IL-6, TNF-alpha, and HGF levels. The peritoneal transport property did not influence inflammatory cytokine and adipokine levels. In conclusion, there was a close relationship between proinflammatory cytokines and adipokines. HGF correlated with proinflammatory cytokines but not with adipokines. The PD-related factors such as RKF, peritoneal property and dialysis glucose load affected levels of proinflammatory cytokines. Body mass index was an important determinant of leptin and adiponectin in PD patients.

A W-band (75 ? 110 GHz) quasi-TEM square waveguide is designed and realized utilizing two-dimensional electromagnetic crystal (EMXT) surfaces as its boundary walls. Because EMXT surfaces provide special boundary conditions, the waveguide size is not limited by the typical cut-off frequency associated with a regular metallic waveguide and free space like wave propagation can be achieved for both polarizations. Both eigenmode and full-wave EM simulations verify the quasi-TEM propagation at the designed frequencies. The S-parameters of the EMXT waveguide in a WR-10 fixture is measured and low insertion loss that agrees with simulation is obtained. This type of waveguides may be useful for applications including spatial power combining, low loss interconnects, and packaging for millimeter wave systems.

Macrophage accumulation in the arterial wall and smooth muscle cell (SMC) proliferation are features of type 2 diabetes mellitus (DM) and its vascular complications. However, the effects of diabetic monocyte-derived macrophages on vascular SMC proliferation are not clearly understood. In the present study, we investigated the pro-proliferative effect of macrophages isolated from DM patients on vascular SMCs. Macrophage-conditioned media (MCM) were prepared from macrophages isolated from DM patients. DM-MCM treatment induced HASMC proliferation, decreased p21(Cip1) and p27(Kip1) expressions, and increased microRNA (miR)-17-5p and miR-221 expressions. Inhibition of either miR-17-5p or miR-221 inhibited DM-MCM-induced cell proliferation. Inhibition of miR-17-5p abolished DM-MCM-induced p21(Cip1) down-regulation; and inhibition of miR-221 attenuated the DM-MCM-induced p27(Kip1) down-regulation. Furthermore, blocking assays demonstrated that PDGF-CC in DM-MCM is the major mediators of cell proliferation in SMCs. In conclusion, our present data support the hypothesis that SMC proliferation stimulated by macrophages may play critical roles in vascular complications in DM patients and suggest a new mechanism by which arterial disease is accelerated in diabetes.

To analyze the clinical features, causative pathogens and therapeutic outcomes of bacterial meningitis in hemodialyzed patients.Two hundred and sixty-seven patients,or = 16 yrs, were identified with culture-proven bacterial meningitis. In addition, the causative pathogens and therapeutic outcomes between uremic and non-uremic patients with adult bacterial meningitis were analyzed.Nine uremic patients with bacterial meningitis, accounting for 3% (9/267) of our adult patients with culture-proven bacterial meningitis had fever, disturbed consciousness and seizures. These were the three most common manifestations in our patients. The interval between the onset of symptoms and therapy start was 5-11 days (mean: 9 days). No patients were initially diagnosed with bacterial meningitis, two patients were initially suspected of having infection of unknown origin. In the non-uremic patient group, klebsiella pneumoniae, Staphylococcus aureus, and Streptococcus pneumoniae were the most frequently detected pathogens, while pseudomonas aeruginosa and coagulase-negative Staphylococcus were the most prevalent in the uremic patients group. The overall mortality rates for the non-uremic and uremic patient groups were 33 and 78% respectively.The mortality rate for bacterial meningitis in the uremic patients group remained high. Due to non-specific manifestations and slow evolution, bacterial meningitis was commonly misdiagnosed as uremic encephalopathy. Therefore, effective treatment was usually delayed. To avoid treatment failure, early diagnosis, careful monitoring of clinical condition and appropriate antibiotic choices are necessary.

PURPOSE: The biofragmentable anastomotic ring (BAR) is now accepted as an alternative anastomotic method to handsewn and stapled anastomosis in colonic surgery. However, for a short rectal stump in a narrow pelvis, it is rather difficult to use the BAR in a low anterior resection. METHOD: To overcome the difficulty, we designed and used a BAR-adapter to facilitate biofragmentable ring anastomosis following low anterior resection in eight patients with rectal cancers. RESULTS: There was no case in our series having received conversion to other methods. There was no significant complication associated with this technique. CONCLUSION: With the BAR-adapter, the applicability of the BAR can be greatly expanded in colorectal anastomosis following low anterior resection.

PURPOSE: The biofragmentable anastomotic ring remains difficult to use for low rectal anastomosis. The authors report their experience of clinical application of the biofragmentable ring in low anterior resection with a newly designed instrument. METHODS: In this series, 31 patients underwent sphincter-preserving low anterior resections for rectal tumors from May 1993 to November 1994. With the assistance of a self-developed anastomotic instrument (biofragmentable anastomotic ring gun), biofragmentable ring anastomoses were performed following low anterior resection. RESULTS: There was no operative mortality. One patient had clinical evidence of anastomotic leakage. In postoperative follow-up, there was no anastomotic stenosis or incontinence. CONCLUSION: Therefore, we believe biofragmentable ring rectal anastomosis is a safe and reliable alternative to other anastomotic methods in rectal surgery.

Ras oncogene and p53 gene mutations are frequently observed in colorectal cancers. The role of co-operation between these two genes in the tumorigenesis of colorectal cancer was evaluated. Point mutations in K-ras oncogene and hotspot codons of p53 gene of colorectal cancers were evaluated by naturally created or amplified created restriction site method. Nine of 42 cases (21.4%) of colorectal cancer showed K-ras oncogene mutations. Six of 42 cases (14.3%) of colorectal cancer showed p53 gene hotspot point mutations. The low frequency of p53 gene mutation in this series may be due to racial difference or different hotspot codons. When six cases with mutated p53 gene were examined, only one (16.7%) showed concurrent K-ras oncogene codon 12 and p53 gene codon 248 mutations. We concluded that the co-operation between ras oncogene and p53 gene hotspot point mutations in the tumorigenesis of colorectal cancer in Chinese was not common. Other factors such as adenomatous polyposis coli gene mutations, oncogene activation or tumour suppression gene inactivation may be involved.

In this study, we obtained saturated deep-blue electroluminescence (EL) from solid state light-emitting electrochemical cells (LECs) incorporating the ionic terfluorene derivative 1, which we synthesized through covalent tethering of methylimidazolium moieties as pendent groups of terfluorene. Compound 1 exhibited the deep-blue emission, extremely high quantum yield, and reversible redox behavior that are characteristic of terfluorene derivatives. LEC devices incorporating terfluorene 1 exhibited deep-blue EL with CIE coordinates of (0.159, 0.115) and (0.151, 0.122) in the absence and presence, respectively, of the ionic liquid (IL) BMIM·PF6. The peak external quantum efficiency and peak power efficiency of 1 in the presence of the IL reached 1.14% and 1.24 lm W−1, respectively. These CIE coordinates are the most saturated blue emissions ever reported for LECs.

Background Homocysteine and pro-inflammatory mediators such as cyclooxygenase-2 (COX-2) have been linked to vascular dysfunction and risks of cardiovascular diseases. Fulvic acid (FA), a class of compounds of humic substances, possesses various pharmacological properties. However, the effect of FA on inflammatory responses of the monocytes remains unclear. We investigated the regulatory effect of FA on homocysteine-induced COX-2 expression in human monocytes. Methods Peripheral blood monocytes and U937 cells were used for all experiments. Real-time PCR and ELISA assay were used to analyze the COX-2 mRNA expression and PGE2 secretion, respectively. Specific inhibitors were used to investigate the mechanism of homocysteine-mediating COX-2 mRNA expression and PGE2 secretion. Luciferase assay, transcription factor ELISA, and chromatin immunoprecipitation were used to determine the role of nuclear factor-κB in FA-mediated inhibition of homocysteine effect on monocytes. Results The results show that pretreating monocytes with FA inhibited the homocysteine-induced COX-2 expression in a dose-dependent manner. Stimulation of U937 monocytes with homocysteine induced rapid increases in the phosphorylation of ERK and JNK; the inhibitor for ERK and JNK attenuated the homocysteine-induced nuclear factor-κB activation and COX-2 expression. Transcription factor ELISA and chromatin immunoprecipitation assays showed that FA blocked the homocysteine-induced increases in the binding activity and in vivo promoter binding of nuclear factor-κB in monocytes. Conclusions Our findings provide a molecular mechanism by which FA inhibits homocysteine-induced COX-2 expression in monocytes, and a basis for using FA in pharmaceutical therapy against inflammation.