The ability to detect the presence of human papillomavirus (HPV)-DNA sequences in urine was evaluated using polymerase chain reaction (PCR). DNA was purified and extracted from urine samples, and subjected to 40 cycles of amplification using the consensus primer pair MY11 and MY09. Coamplification using the beta-globin primers, GH20 and PC04, was performed as an internal reaction control. Following assay optimization, urine samples from 22 women undergoing examination for cervical dysplasia were tested for the presence of HPV-DNA. PCR assay results were correlated with cytologic and histologic findings as well as ViraType assay results. Overall, HPV was detected by PCR in 16 (76%) of the interpretable samples. HPV sequences were detected in 13 (87%) of the 15 specimens from women showing evidence of condylomata, dysplasia, or invasive carcinoma. HPV was detected in 3 (50%) of the women whose cytologic or histologic results were either negative or showed benign atypia. Although the sample size in this study is small, our results show that HPV can be detected by PCR in a majority of individuals showing evidence of HPV infection. The method described provides a means for the clinical laboratory to detect a broad range of HPV types from using a sample obtained by noninvasive techniques. The ability to easily obtain urine would allow for increased numbers of individuals to be tested, and thus, aid in our understanding of HPV.
Ventilator-induced lung injury (VILI) is a significant risk for patients with acute respiratory distress syndrome (ARDS). Management of the ARDS patient is currently dominated by the use of low tidal volume mechanical ventilation, the presumption being that this mitigates overdistension (OD) injury to the remaining normal lung tissue. Evidence exists, however, that it may be more important to avoid cyclic recruitment and derecruitment (RD) of lung units, although the relative roles of OD and RD in VILI remain unclear. Forty pigs had a heterogeneous lung injury induced by Tween instillation and were randomized into four groups (n = 10 each) with higher (↑) or lower (↓) levels of OD and/or RD imposed using airway pressure release ventilation (APRV). OD was increased by setting inspiratory airway pressure to 40 cmH2O and lessened with 28 cmH2O. RD was attenuated using a short duration of expiration (~0.45 s) and increased with a longer duration (~1.0 s). All groups developed mild ARDS following injury. RD↑OD↑ caused the greatest degree of lung injury as determined by PaO2/FiO2 ratio (226.1±41.4mmHg). RD↑OD↓ (PaO2/FiO2 = 333.9 ± 33.1 mmHg) and RD↓OD↑ (PaO2/FiO2 = 377.4 ± 43.2 mmHg) were both moderately injurious, while RD↓OD↓ (PaO2/FiO2 = 472.3±22.2mmHg; p<0.05) was least injurious. Both tidal volume and driving pressure were essentially identical in the RD↑OD↓ and RD↓OD↑ groups. We therefore conclude that considerations of expiratory time may be at least as important as pressure for safely ventilating the injured lung.
Multidrug-resistant organisms are increasing in healthcare settings, and there are few antimicrobials available to treat infections from these bacteria . Pseudomonas aeruginosa is an opportunistic pathogen in burn patients and individuals with cystic fibrosis (CF), and a leading cause of nosocomial infections. P. aeruginosa is inherently resistant to many antibiotics and can develop resistance to others, limiting treatment options. P. aeruginosa has multiple sigma factors to regulate transcription. The alternative sigma factor, RpoN (σ 54 ), regulates many virulence genes and is linked to antibiotic resistance. Recently, we described a cis-acting peptide, RpoN*, which is a “molecular roadblock”, binding consensus promoters at the -24 site, blocking transcription. RpoN* reduces virulence of P. aeruginosa laboratory strains, but its effects in clinical isolates was unknown. We investigated the effects of RpoN* on phenotypically varied P. aeruginosa strains isolated from CF patients. RpoN* expression reduced motility, biofilm formation, and pathogenesis in a P. aeruginosa-C. elegans infection model. Furthermore, we investigated RpoN* effects on antibiotic susceptibility in a laboratory strain. RpoN* expression increased susceptibility to several beta-lactam-based antibiotics in strain P. aeruginosa PA19660 Xen5 . We show that using a cis-acting peptide to block RpoN consensus promoters has potential clinical implications in reducing virulence and improving antibiotic susceptibility.
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