Infrared luminosities and aromatic features in the 24 μm flux-limited sample of 5muses

We study a 24 μm selected sample of 330 galaxies observed with the infrared spectrograph for the 5 mJy Unbiased Spitzer Extragalactic Survey. We estimate accurate total infrared luminosities by combining mid-IR spectroscopy and mid-to-far infrared photometry, and by utilizing newempirical spectral templates from Spitzer data. The infrared luminosities of this sample range mostly from 10^9 L_⊙ to 10^(13.5) L_⊙,with 83% in the range 10^(10) L_⊙ < L_(IR) < 10^(12) L_⊙. The redshifts range from 0.008 to 4.27, with a median of 0.144. The equivalent widths of the 6.2 μm aromatic feature have a bimodal distribution, probably related to selection effects. We use the 6.2μm polycyclic aromatic hydrocarbon equivalent width (PAH EW) to classify our objects as starburst (SB)-dominated (44%), SB-AGN composite (22%), and active galactic nucleus (AGN)-dominated (34%). The high EW objects (SB-dominated) tend to have steeper mid-IR to far-IR spectral slopes and lower L_(IR) and redshifts. The low EW objects (AGN-dominated) tend to have less steep spectral slopes and higher L_(IR) and redshifts. This dichotomy leads to a gross correlation between EW and slope, which does not hold within either group. AGN-dominated sources tend to have lower log(L_(PAH7.7 μm)/L_(PAH11.3 μm)) ratios than star-forming galaxies, possibly due to preferential destruction of the smaller aromatics by the AGN. The log(L_(PAH7.7 μm)/L_(PAH11.3 μm)) ratios for star-forming galaxies are lower in our sample than the ratios measured from the nuclear spectra of nearby normal galaxies, most probably indicating a difference in the ionization state or grain size distribution between the nuclear regions and the entire galaxy. Finally, we provide a calibration relating the monochromatic continuum or aromatic feature luminosity to L_(IR) for different types of objects

Chromosome 3 Anomalies Investigated by Genome Wide SNP Analysis of Benign, Low Malignant Potential and Low Grade Ovarian Serous Tumours

Ovarian carcinomas exhibit extensive heterogeneity, and their etiology remains unknown. Histological and genetic evidence has led to the proposal that low grade ovarian serous carcinomas (LGOSC) have a different etiology than high grade carcinomas (HGOSC), arising from serous tumours of low malignant potential (LMP). Common regions of chromosome (chr) 3 loss have been observed in all types of serous ovarian tumours, including benign, suggesting that these regions contain genes important in the development of all ovarian serous carcinomas. A high-density genome-wide genotyping bead array technology, which assayed >600,000 markers, was applied to a panel of serous benign and LMP tumours and a small set of LGOSC, to characterize somatic events associated with the most indolent forms of ovarian disease. The genomic patterns inferred were related to TP53, KRAS and BRAF mutations. An increasing frequency of genomic anomalies was observed with pathology of disease: 3/22 (13.6%) benign cases, 40/53 (75.5%) LMP cases and 10/11 (90.9%) LGOSC cases. Low frequencies of chr3 anomalies occurred in all tumour types. Runs of homozygosity were most commonly observed on chr3, with the 3p12-p11 candidate tumour suppressor region the most frequently homozygous region in the genome. An LMP harboured a homozygous deletion on chr6 which created a GOPC-ROS1 fusion gene, previously reported as oncogenic in other cancer types. Somatic TP53, KRAS and BRAF mutations were not observed in benign tumours. KRAS-mutation positive LMP cases displayed significantly more chromosomal aberrations than BRAF-mutation positive or KRAS and BRAF mutation negative cases. Gain of 12p, which harbours the KRAS gene, was particularly evident. A pathology review reclassified all TP53-mutation positive LGOSC cases, some of which acquired a HGOSC status. Taken together, our results support the view that LGOSC could arise from serous benign and LMP tumours, but does not exclude the possibility that HGOSC may derive from LMP tumours

Unilateral vocal fold immobility: a tertiary hospital's experience over 5 years.

The objective of the study was to determine the etiology and subsequent management of patients with unilateral vocal fold immobility (UVFI) and compare our results with other such studies. This was a retrospective case series of all patients that were treated for UVFI at one single tertiary referral centre between 2010 and 2014. The medical records of 161 patients over a 5-year period diagnosed with UVFI were analyzed. We looked at the patient demographics, side of immobility, etiology, management and voice assessment. A total of 21 patients were excluded due to varying reasons including second presentation and incomplete data. Our results demonstrated 37.1% of cases to be due to non-thyroid surgery (mainly vascular or anterior cervical spine surgery) compared to thyroid or parathyroid (18.6%). Carotid endarterectomy was the commonest cause followed by cervical spine discectomy or fusion. Other iatrogenic causes included thoracic surgery either involving the lung or not. Our results are very much in keeping with those seen by our colleagues in North America. A better appreciation of the causes of UVFI especially in cases not performed by otolaryngologists and head and neck surgeons should be highlighted and the necessary steps should be taken to prevent this iatrogenic complication