The Role of Positron Emission Tomography/Computed Tomography Imaging in Head and Neck Cancer after Radical Chemoradiotherapy: a Single Institution Experience.

AIMS: Positron emission tomography/computed tomography (PET/CT) is used to restage head and neck cancer 3 months after chemoradiotherapy. The purpose of this study was to determine the negative predictive value (NPV) of a scan reported as having no abnormal uptake and the positive predictive values (PPV) for different maximum standardised uptake value (SUVmax) thresholds. MATERIALS AND METHODS: Patients with squamous cell carcinoma of the oro-/hypopharynx/larynx (n = 206) were included. SUVmax and subsequent locoregional recurrence were documented. RESULTS: The median SUVmax was 11.2 (range 4-33)/4.6 (range 2-30), respectively, in patients with/without definite primary site recurrence (P = 0.004). The median SUVmax was 4.4 (range 2.6-15.6)/3.1 (range 2.1-4.6), respectively, in patients with/without definite nodal recurrence (P = 0.003). The NPV for a scan reported as having no abnormal uptake was 92%. The PPV for the SUVmax thresholds 4, 6 and 8, respectively, were 53, 65 and 92% (primary site) and 93, 100 and 100% (nodes). CONCLUSIONS: The NPV of PET/CT after chemoradiation is consistent with the literature and underlines the importance of PET/CT in restaging the primary site if salvage neck dissection is considered. The overall PPV of PET/CT remains low but is high for nodal SUVmax > 4. These data could be used to design risk-stratified follow-up schedules.

MYO1F as a candidate gene for nonsyndromic deafness, DFNB15.

BACKGROUND: Earlier studies have mapped the autosomal recessive nonsyndromic deafness locus, DFNB15, to chromosomes 3q21.3-q25.2 and 19p13.3-13.1, identifying one of these chromosomal regions (or possibly both) as the site of a deafness-causing gene. Mutations in unconventional myosins cause deafness in mice and humans. One unconventional myosin, myosin 1F (MYO1F), is expressed in the cochlea and maps to chromosome 19p13.3-13.2. OBJECTIVE: To evaluate MYO1F as a candidate gene for deafness at the DFNB15 locus by determining its genomic structure and screening each exon for deafness-causing mutations to identify possible allele variants of MYO1F segregating in the DFNB15 family. METHODS: We used radiation hybrid mapping to localize MYO1F on chromosome arm 19p. We next determined its genomic structure using multiple long-range polymerase chain reaction experiments. Using these data, we completed mutation screening using single-stranded conformational polymorphism analysis and direct sequencing of affected and nonaffected persons in the original DFNB15 family. RESULTS: Radiation hybrid mapping placed MYO1F in the DFNB15 interval, establishing it as a positional candidate gene. Its genomic structure consists of 24 coding exons. No mutations or genomic rearrangements were found in the original DFNB15 family, making it unlikely that MYO1F is the disease-causing gene in this kindred. CONCLUSIONS: Although we did not find MYO1F allele variants in one family with autosomal recessive nonsyndromic hearing loss, the gene remains an excellent candidate for hereditary hearing impairment. Given its wide tissue expression, MYO1F might cause syndromic deafness.

Fluconazole concentrations in pulmonary tissue and pericardial fluid.

In order to investigate the clinical efficacy of the triazole antifungal agent fluconazole (FCA) in the treatment of pulmonary mycosis, in the present study the concentrations of fluconazole in human pulmonary tissue, pericardial fluid and serum were determined at 1, 2, 12 and 13 h after intravenous administration of fluconazole 200 mg. The mean FCA concentrations in the serum were 4.04 mg/l (1 h), 3.82 mg/l (2 h), 2.35 mg/l (12 h) and 2.13 mg/l (13 h). The respective FCA levels in the pulmonary tissue were 4.64 mg/kg, 4.54 mg/kg; 3.50 mg/kg and 3.40 mg/kg and the concentrations in the pericardial fluid were 3.86 mg/l, 3.57 mg/l, 2.35 mg/l and 2.13 mg/l. The FCA concentrations in the pulmonary tissue that were statistically significant higher than the serum concentrations were found at 2 h, 12 h and 13 h after intravenous administration (p < 0.05).

The influence of verapamil on lung preservation. A study on rabbit lungs with a reperfusion model allowing physiological loading.

Calcium-channel blockers have recently been shown to improve myocardial and renal preservation. It was presumed that this should apply also for donor lungs. Extracorporeal reperfusion models have proved to be particularly useful for the experimental assessment of donor-lung preservation techniques. One disadvantage of the models employed to date is that with the low reperfusion rates used, any minimal lung damage is compensated for and is thus not detected or at least not detected promptly. The aim of this study was the investigation of the effect of verapamil in a modified reperfusion model with physiological volume/time flow ratio during reperfusion. The application of verapamil into the flush and into the reperfusion blood of an ex-vivo lung transplantation model renders, particularly after 12 hr of preservation, a statistically significant improvement of the organ function.

A modified ex-vivo rabbit lung reperfusion model for the study of lung preservation techniques.

Extracorporeal reperfusion models have proved to be particularly useful for the experimental assessment of donor lung preservation techniques. One disadvantage of the models employed to date is what with the low reperfusion rates used, any minimal lung damage is compensated for and is thus not detected or at least not detected promptly. By permitting reperfusion at physiological flow rates, use of a membrane deoxygenator in a closed circuit permits early detection of damage due to ischaemia or reperfusion. A modified ex-vivo reperfusion model is presented which permits assessment of lung function under almost physiological conditions after varying periods of ischaemia and varying conditions of preservation.