Robotic-assisted ureteral reimplantation with Boari flap and psoas hitch: a single-institution experience.

Robotic-assisted ureteral reimplantations were performed on 3 patients at a single institution, 2 with Boari flap and psoas hitch and 1 with psoas hitch alone. These were for urothelial carcinoma of the distal ureter, ureteral obstruction caused by distal ureteral endometriosis, and ureteral transaction during gynecologic surgery. We used intraoperative ureteroscopy to confirm tumor margins as well as a simple technique for retrograde placement of transvesicle wire prior to ureteral anastomosis. Surgery and recovery were uneventful. This illustrates that robotic-assisted ureteral reimplantation with Boari flap and psoas hitch is a safe and viable approach for ureterovesicle reconstruction.

Does an oral appliance reduce palatal flutter and tongue base snoring?

OBJECTIVES: Oral appliances are designed to treat snoring and sleep apnea by advancing the mandible and tongue. We test the hypothesis that an oral appliance affects palatal snoring as well as tongue base obstruction. METHODS: Prospective observational cohort study. Sixty patients with a chief complaint of snoring with or without apnea were enrolled. Each patient underwent a home sleep test followed by 3 weeks sleeping with an oral appliance. Each patient then underwent a repeat home sleep test while using the device. RESULTS: There was a statistically significant improvement in the snores per hour (P = 0.0005), the maximum snoring loudness (P = 0.0001), average snoring loudness (P = 0.00001), and the percentage of palatal snoring (P = 0.0007). There was also a significant decrease in oxygen desaturation events (P = 0.003). CONCLUSIONS: This study suggests oral appliances may be effective treatment for both palatal and tongue base snoring.

Biphasic regulation by bile acids of dermal fibroblast proliferation through regulation of cAMP production and COX-2 expression level.

We have previously reported that the bile acids chenodeoxycholate (CDCA) and ursodeoxycholate (UDCA) decreased PGE1-induced cAMP production in a time- and dose-dependent manner not only in hepatocytes but also in nonhepatic cells, including dermal fibroblasts. In the present study, we investigated the physiological relevance of this cAMP modulatory action of bile acids. PGE1 induced cAMP production in a time- and dose-dependent manner. Moreover, PGE1 (1 microM), forskolin (1-10 microM), and the membrane-permeable cAMP analog CPT-cAMP (0.1-10 microM) decreased dermal fibroblast proliferation in a dose-dependent manner with a maximum inhibition of approximately 80%. CDCA alone had no significant effect on cell proliferation at a concentration up to 25 microM. However, CDCA significantly reduced PGE1-induced cAMP production by 80-90% with an EC(50) of approximately 20 microM. Furthermore, at concentrations < or =25 microM, CDCA significantly attenuated the PGE-1-induced decreased cell proliferation. However, at concentrations of 50 microM and above, while still able to almost completely inhibit PGE-1-induced cAMP production, CDCA, at least in part through an increased cyclooxygenase-2 (COX-2) expression level and PGE2 synthesis, produced a direct and significant decrease in cell proliferation. Indeed, the CDCA effect was partially blocked by approximately 50-70% by both indomethacin and dexamethasone. In addition, overexpression of COX-2 cDNA wild type resulted in an increased efficacy of CDCA to block cell proliferation. The effects of CDCA on both cAMP production and cell proliferation were similar to those of UDCA and under the same conditions cholate had no effect. Results of the present study underline pathophysiological consequences of cholestatic hepatobiliary disorders, in which cells outside of the enterohepatic circulation can be exposed to elevated bile acid concentrations. Under these conditions, low bile acid concentrations can attenuate the negative hormonal control on cell proliferation, resulting in the stimulation of cell growth, while at high concentrations these bile acids provide for a profound and prolonged inhibition of cell proliferation.

Total nasopharyngeal stenosis: treatment with laser excision, nasopharyngeal obturators, and topical mitomycin-c.

OBJECTIVE: Severe nasopharyngeal stenosis after uvulopalatopharyngoplasty (UPPP) is a dreaded complication. Very little has been written about successful treatment because attempts at correction frequently fail. Severe stenosis of the nasopharynx drastically worsens speech, swallowing, and obstructive sleep apnea (OSA). We present our successful experience with severe stenosis focusing on a simple functional repair using topical mitomycin-c as well as differing daytime and nighttime palatal obturators. METHODS: Three adults with total or near-total nasopharyngeal stenosis secondary to UPPP were referred to our institution after multiple failed attempts at repair. Each presented with significant OSA on polysomnogram (PSG), with excessive daytime somnolence and voice and swallowing complaints. Under general anesthesia, a CO2 laser is used to create an opening in the nasopharynx. Removable and adjustable palatal obturators are fashioned to keep the nasopharynx open with a daytime insert piece with a small obturator hole for diminished velopharyngeal insufficiency and a nighttime piece without an insert to maximize recumbent airflow. Obturators are removed 6 months later with topical application of mitomycin-c as a fibroblast inhibitor. All patients were followed clinically for at least 1 year and received posttreatment PSG. RESULTS: All patients experienced resolution of their stenoses. Swallowing and voice complaints resolved. Either OSA was eliminated or any residual OSA was successfully treated with nasal continuous positive airway pressure. Serial videoendoscopic images throughout the treatment phase demonstrate the effectiveness of this new technique. CONCLUSIONS: Severe nasopharyngeal stenosis is a rare but devastating complication of UPPP. We introduce a simple technique that uses functional palatal obturators and topical mitomycin-c and describe our success with this treatment algorithm.

Tetracycline resistance in Chlamydia suis mediated by genomic islands inserted into the chlamydial inv-like gene.

Many strains of Chlamydia suis, a pathogen of pigs, express a stable tetracycline resistance phenotype. We demonstrate that this resistance pattern is associated with a resistance gene, tet(C), in the chlamydial chromosome. Four related genomic islands were identified in seven tetracycline-resistant C. suis strains. All resistant isolates carry the structural gene tet(C) and the tetracycline repressor gene tetR(C). The islands share significant nucleotide sequence identity with resistance plasmids carried by a variety of different bacterial species. Three of the four tet(C) islands also carry a novel insertion sequence that is homologous to the IS605 family of insertion sequences. In each strain, the resistance gene and associated sequences are recombined into an identical position in a gene homologous to the inv gene of the yersiniae. These genomic islands represent the first examples of horizontally acquired DNA integrated into a natural isolate of chlamydiae or within any other obligate intracellular bacterium.