A comparison of the cytologic and histologic features of meningiomas in four dogs

Abstract: The cytologic and histologic features of 2 intracranial and 2 spinal (extramedullary cervical) canine meningiomas were compared. Cerebrospinal fluid analysis in 2 cases revealed mild, mixed cell pleocytosis, primarily composed of small lymphocytes and monocytoid cells, with a moderate increase in total protein concentration. Cytologic features suggestive of meningioma included cells with both epithelial and mes-enchymal characteristics and a tendency towards cell clustering. Tumor location also was useful in making a diagnosis. The 4 meningiomas differed histologically from one another, and included angioblastic, psam-momatous, meningotheliomatous, and microcystic anaplastic types, which conformed to a classification scheme for human meningiomas. The classification scheme could not be applied to cytologic specimens.     

Resolution of chylothorax after resection of rib chondroma in a dog

A six-year-old, male dobermann was presented with a history of dyspnoea and bouts of coughing. Radiography and computed tomography of the thorax showed pleural effusion and a well-circumscribed, calcified mass of 10 cm in diameter, appearing to originate from the left first rib. Thoracocentesis revealed that the pleural fluid was chylous in nature. An incisional biopsy was performed, which gave a histological diagnosis of chondroma. Resolution of the chylothorax after en-bloc surgical removal of the tumour suggested that the rib tumour was the initiating cause of the chylothorax. Seventeen months later, rib neoplasia recurred without pleural effusion, and was removed successfully. To the authors' knowledge, rib chondroma, which is an unusual tumour in dogs, has not been previously documented as a cause of chylothorax.     

A systematic survey of loss-of-function variants in human protein-coding genes

Genome-sequencing studies indicate that all humans carry many genetic variants predicted to cause loss of function (LoF) of protein-coding genes, suggesting unexpected redundancy in the human genome. Here we apply stringent filters to 2951 putative LoF variants obtained from 185 human genomes to determine their true prevalence and properties. We estimate that human genomes typically contain ~100 genuine LoF variants with ~20 genes completely inactivated. We identify rare and likely deleterious LoF alleles, including 26 known and 21 predicted severe disease-causing variants, as well as common LoF variants in nonessential genes. We describe functional and evolutionary differences between LoF-tolerant and recessive disease genes and a method for using these differences to prioritize candidate genes found in clinical sequencing studies.