Anatomic factors affecting the use of ultrasound to predict vocal fold motion: A pilot study

Purpose

Ultrasonography is a well-established modality for visualization of head and neck anatomy. Using ultrasound to detect vocal fold mobility has been described before, but no study has evaluated factors affecting the exam reliability. The aim of the study is to determine anatomic factors influencing the reliability of ultrasound to detect vocal fold motion.Methods and materialsPatients underwent ultrasound evaluation and flexible laryngoscopy to assess vocal fold motion from August 2015 to March 2016. Length, accuracy, and clarity of ultrasound examination were assessed, compared to flexible laryngoscopy. For patients with prior neck CT scan imaging, laryngeal anatomy was independently assessed by a blinded neuroradiologist.

Neutron fluence and kerma spectra of a p(66)/Be(40) clinical source.

High-resolution neutron fluence spectra have been measured in the National Accelerator Centre's p(66)/Be(40) neutron therapy beam by the pulsed-beam time-of-flight method. ICRU muscle kerma spectra have been derived from the fluence spectra. Spectral changes resulting from different irradiation conditions have been quantified in terms of the average neutron energy and the fractional low-energy (< 16 MeV) contribution. The changes observed with different thicknesses of polyethylene filtration are consistent with changes in quality parameters determined in biological and microdosimetric experiments. The dosimetry parameters (KtissueA150) N and (Wgas) N calculated for the measured spectra agree with the values recommended in the neutron dosimetry protocol. The shapes of the present fluence spectra differ from previous measurements of p(> 40)/Be spectra. In particular, they differ significantly from the spectrum measured by recoil techniques in an identical neutron therapy unit at the Clatterbridge Hospital, UK. The reasons for the difference are not known.     

Fatal Mycobacterium bovis BCG Infection in TNF-LT-α-Deficient Mice

Neutralization of TNF or disruption of TNF-R1 leads to fatal Mycobacterium bovis BCG infection. Here we used TNF-LT-α-deficient mice to test whether a complete disruption of TNF and LT-α reduces further host resistance to BCG infection. The bacterial burden especially in the lungs of TNF-LT-α-deficient mice was significantly increased and the mice succumbed to infection between 8 and 10 weeks. In the absence of TNF-LT-α the granulomatous response was severely impaired and delayed. The cells in the granulomas of TNF-LT-α-deficient mice expressed low levels of MHC class II and ICAM-1. They contained a few T cells and F4/80-positive macrophages expressing little iNOS and acid phosphatase activity. By contrast, the lethal action of endotoxin was dramatically reduced in BCG-infected TNF-LT-α-deficient mice. In summary, in the absence of TNF-LT-α the recruitment and activation of mononuclear cells in response to BCG infection were significantly delayed and reduced resulting in immature granulomas allowing uncontrolled fatal infection.     

Red flags and religious coping: Identifying some religious warning signs among people in crisis

This study attempts to identify some of the signs of ineffective religious involvement in coping. Drawing from a process/integration model of efficacious coping, three broad types of religious warning signs were defined and 11 subscales were developed. These subscales were administered to a group of Roman Catholic church members and two groups of college undergraduates who had experienced different types of negative life events in the past two years. Statistical analyses were conducted to determine the relationship between these subscales and measures of general mental health and event specific outcome. The theoretical and practical implications of these results are considered. © 1998 John Wiley & Sons, Inc. J Clin Psychol 54: 77–89, 1998.     

Mutations in 2 distinct genetic pathways result in cerebral cavernous malformations in mice

Cerebral cavernous malformations (CCMs) are a common type of vascular malformation in the brain that are a major cause of hemorrhagic stroke. This condition has been independently linked to 3 separate genes: Krev1 interaction trapped (KRIT1), Cerebral cavernous malformation 2 (CCM2), and Programmed cell death 10 (PDCD10). Despite the commonality in disease pathology caused by mutations in these 3 genes, we found that the loss of Pdcd10 results in significantly different developmental, cell biological, and signaling phenotypes from those seen in the absence of Ccm2 and Krit1. PDCD10 bound to germinal center kinase III (GCKIII) family members, a subset of serine-threonine kinases, and facilitated lumen formation by endothelial cells both in vivo and in vitro. These findings suggest that CCM may be a common tissue manifestation of distinct mechanistic pathways. Nevertheless, loss of heterozygosity (LOH) for either Pdcd10 or Ccm2 resulted in CCMs in mice. The murine phenotype induced by loss of either protein reproduced all of the key clinical features observed in human patients with CCM, as determined by direct comparison with genotype-specific human surgical specimens. These results suggest that CCM may be more effectively treated by directing therapies based on the underlying genetic mutation rather than treating the condition as a single clinical entity.     

Clinical value of supine and upright myocardial perfusion imaging in obese patients using the D-SPECT camera

Purpose

We have assessed whether additional upright imaging increases the confidence of interpretation of stress only supine myocardial perfusion imaging (MPI) in obese patients.

Methods and results

Tc-MIBI stress MPI of 101 consecutive patients (M = 49, 62 ± 12 years) with BMI ≥30 scanned on the D-SPECT cardiac camera were assessed. Images were interpreted as diagnostic or equivocal and the need for a rest study was recorded. Stress supine MPI was interpreted first, then gated and finally upright data were added. Defects on supine but not on upright were defined as artefacts and defects seen on both as abnormal. The total perfusion deficit (TPD) was also quantified. There were 27 normal, 22 abnormal, and 52 equivocal supine scans. The median EF was 52%, unaffecting the need for rest imaging. Upright imaging reclassified 32/52 (62%) equivocal studies as normal and 6/52 (11%) as abnormal (P < 0.001). Rest scan was deemed needed in 74/101 patients on supine vs 42/101 on supine/upright (P < 0.001). Supine TPD was normal in 53 and supine/upright TPD was normal in 70 patients (P < 0.001).

Conclusion

Supine stress MPI is inadequate in obese patients. The addition of upright imaging significantly increases the ability to interpret scans as diagnostic and may reduce considerably the need for rest imaging.     

Fulvene-5 potently inhibits NADPH oxidase 4 and blocks the growth of endothelial tumors in mice

Hemangiomas are the most common type of tumor in infants. As they are endothelial cell–derived neoplasias, their growth can be regulated by the autocrine-acting Tie2 ligand angiopoietin 2 (Ang2). Using an experimental model of human hemangiomas, in which polyoma middle T–transformed brain endothelial (bEnd) cells are grafted subcutaneously into nude mice, we compared hemangioma growth originating from bEnd cells derived from wild-type, Ang2^+/–, and Ang2^–/– mice. Surprisingly, Ang2-deficient bEnd cells formed endothelial tumors that grew rapidly and were devoid of the typical cavernous architecture of slow-growing Ang2-expressing hemangiomas, while Ang2^+/– cells were greatly impaired in their in vivo growth. Gene array analysis identified a strong downregulation of NADPH oxidase 4 (Nox4) in Ang2^+/– cells. Correspondingly, lentiviral silencing of Nox4 in an Ang2-sufficient bEnd cell line decreased Ang2 mRNA levels and greatly impaired hemangioma growth in vivo. Using a structure-based approach, we identified fulvenes as what we believe to be a novel class of Nox inhibitors. We therefore produced and began the initial characterization of fulvenes as potential Nox inhibitors, finding that fulvene-5 efficiently inhibited Nox activity in vitro and potently inhibited hemangioma growth in vivo. In conclusion, the present study establishes Nox4 as a critical regulator of hemangioma growth and identifies fulvenes as a potential class of candidate inhibitor to therapeutically interfere with Nox function.