Rowland Payne syndrome in a neonate as a consequence of birth trauma

Background: The syndrome of Rowland Payne is a rare triad of unilateral Horner syndrome, ipsilateral vocal cord paralysis, and ipsilateral paralysis of the hemidiaphragm. Case: A healthy newborn was noted to have right ptosis, a weak hoarse cry, and stridor immediately following delivery with forceps. Pupillary miosis on the same side as the ptosis was observed. Chest X-ray showed elevation of the right diaphragmatic dome. A diagnosis of Rowland Payne syndrome was made. Neuroimaging did not reveal any structural mass lesions. The hoarseness and stridor resolved within 1 month without intervention. The Horner syndrome improved but did not disappear completely. Conclusion: In the few reported cases in the literature, the cause of Rowland Payne syndrome has been a malignant lesion of the anterior neck disrupting the oculosympathetic nerve, the vagus nerve, and the phrenic nerve. This is the first report of Rowland Payne syndrome in a neonate. We did not find any malignancy or compressive lesion to account for his symptoms and signs. We suggest that shearing forces at the lower neck at the level of the clavicle caused stretching and mechanical injury to these motor nerves or their branches. In this report of Roland Payne syndrome related to birth trauma, the prognosis was favorable

1864-11-28 Mrs. C.A. Murone inquires about her husband George

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Automation in urinalysis: evaluation of three urine test strip analysers

A clinical laboratory evaluation was conducted on the Clinitek Auto 2000, the Super Aution Analyzer and the Urotron RL9 for the determination of glucose, protein, pH, blood, ketone-bodies and bilirubin

Rowland Payne syndrome in a neonate as a consequence of birth trauma

Background: The syndrome of Rowland Payne is a rare triad of unilateral Horner syndrome, ipsilateral vocal cord paralysis, and ipsilateral paralysis of the hemidiaphragm. Case: A healthy newborn was noted to have right ptosis, a weak hoarse cry, and stridor immediately following delivery with forceps. Pupillary miosis on the same side as the ptosis was observed. Chest X-ray showed elevation of the right diaphragmatic dome. A diagnosis of Rowland Payne syndrome was made. Neuroimaging did not reveal any structural mass lesions. The hoarseness and stridor resolved within 1 month without intervention. The Horner syndrome improved but did not disappear completely. Conclusion: In the few reported cases in the literature, the cause of Rowland Payne syndrome has been a malignant lesion of the anterior neck disrupting the oculosympathetic nerve, the vagus nerve, and the phrenic nerve. This is the first report of Rowland Payne syndrome in a neonate. We did not find any malignancy or compressive lesion to account for his symptoms and signs. We suggest that shearing forces at the lower neck at the level of the clavicle caused stretching and mechanical injury to these motor nerves or their branches. In this report of Roland Payne syndrome related to birth trauma, the prognosis was favorable

Prognostic impact and the relevance of PTEN copy number alterations in patients with advanced colorectal cancer (CRC) receiving bevacizumab

Article first published online: 25 MAR 2013Loss of phosphatase and tensin homologue (PTEN) expression may be prognostic in colorectal cancer (CRC) and may have a correlation with vascular endothelial growth factor (VEGF) expression via hypoxia-inducible factor 1 (HIF-1) alpha, and the PI3K/mTOR pathways. We therefore have explored the prognostic association of PTEN loss and the potential that PTEN loss may be predictive of outcome with bevacizumab. Patients enrolled in the AGITG MAX trial, a randomized Phase III trial of capecitabine (C) +/− bevacizumab (B) (+/− mitomycin C [M]) with available tissues were analyzed for PTEN expression (loss vs. no loss) as assessed using a Taqman® copy number assay (CNA). Of the original 471 patients enrolled, tissues from 302 (64.1%) patients were analyzed. PTEN loss was observed in 38.7% of patients. There was no relationship between PTEN loss and KRAS or BRAF mutation. PTEN status was not prognostic for progression-free survival (PFS) or overall survival (OS) in multivariate analyses adjusting for other baseline factors; loss versus no loss PFS hazard ratio (HR) 0.9 (0.7–1.16), OS HR 1.04 (0.79–1.38). PTEN was not prognostic when assessed by KRAS and BRAF status. By using the comparison of C versus CB+CBM, PTEN status was not significantly predictive of the effectiveness of B for PFS or OS. PTEN status was not prognostic for survival in advanced colorectal cancer, irrespective of KRAS or BRAF status. PTEN status did not significantly predict different benefit with bevacizumb therapy.Timothy J. Price, Jennifer E. Hardingham, Chee K. Lee, Amanda R. Townsend, Joseph W. Wrin, Kate Wilson, Andrew Weickhardt, Robert J. Simes, Carmel Murone & Niall C. Tebbut

Effect of Inhibition of the Lysophosphatidic Acid Receptor 1 on Metastasis and Metastatic Dormancy in Breast Cancer

Background Previous studies identified the human nonmetastatic gene 23 (NME1, hereafter Nm23-H1) as the first metastasis suppressor gene. An inverse relationship between Nm23-H1 and expression of lysophosphatidic acid receptor 1 gene (LPAR1, also known as EDG2 or hereafter LPA1) has also been reported. However, the effects of LPA1 inhibition on primary tumor size, metastasis, and metastatic dormancy have not been investigated. Methods The LPA1 inhibitor Debio-0719 or LPA1 short hairpinned RNA (shRNA) was used. Primary tumor size and metastasis were investigated using the 4T1 spontaneous metastasis mouse model and the MDA-MB-231T experimental metastasis mouse model (n = 13 mice per group). Proliferation and p38 intracellular signaling in tumors and cell lines were determined by immunohistochemistry and western blot to investigate the effects of LPA1 inhibition on metastatic dormancy. An analysis of variance-based two-tailed t test was used to determine a statistically significant difference between treatment groups. Results In the 4T1 spontaneous metastasis mouse model, Debio-0719 inhibited the metastasis of 4T1 cells to the liver (mean = 25.2 liver metastases per histologic section for vehicle-treated mice vs 6.8 for Debio-0719-treated mice, 73.0% reduction, P < .001) and lungs (mean = 6.37 lesions per histologic section for vehicle-treated mice vs 0.73 for Debio-0719-treated mice, 88.5% reduction, P < .001), with no effect on primary tumor size. Similar results were observed using the MDA-MB-231T experimental pulmonary metastasis mouse model. LPA1 shRNA also inhibited metastasis but did not affect primary tumor size. In 4T1 metastases, but not primary tumors, expression of the proliferative markers Ki67 and pErk was reduced by Debio-0719, and phosphorylation of the p38 stress kinase was increased, indicative of metastatic dormancy. Conclusion The data identify Debio-0719 as a drug candidate with metastasis suppressor activity, inducing dormancy at secondary tumor site