Thirteen dogs, including 6 Rottweiler dogs, exhibiting clinical signs of spinal cord dysfunction and myelographically confirmed subarachnoid space enlargement were investigated. To characterize the lesions and to get a better understanding of their pathogenesis, different imaging techniques were used in association with explorative surgical procedures (12 dogs) and histopathologic techniques (5 dogs). All subjects underwent preoperative myelography, five of which were examined by computed tomography (CT) scanning and one by magnetic resonance imaging (MRI) as well as cerebrospinal fluid (CSF) flow measurement (velocimetry). Most animals were <12 months old (7/13 dogs) and Rottweilers were over-represented (6/13 dogs). The lesions were mainly located dorsally with respect to the spinal cord (10/13 dogs) and in the cranial cervical area (8/13 dogs). MRI suggested spinal cord deviation with signs of ventral leptomeningeal adhesion opposite the enlarged space. In one dog, velocimetry confirmed that the "cyst" was freely communicating with the surrounding CSF space. Surgical investigation confirmed leptomeninges-induced ventral adhesion in 4/5 dogs. Follow-up studies, carried out from 6 months to 2.5 years postoperatively, showed there was full recovery in 8/13 dogs. This study suggests that the compression of the spinal cord is possibly not caused by a cyst. Adhesion resulting from a combination of microtrauma and chronic inflammatory processes induces a secondary enlargement of the subarachnoid space and may be a significant causative factor in spinal cord compression and dysfunction. The over-representation of Rottweilers and the young age of the animals in the study suggest a possible genetic predisposition and an inherited etiology.

Sagittal and transverse ultrasonographic images of the prostate gland were obtained in 100 healthy adult intact male dogs. Prostatic length, width, and height on transverse and sagittal images as well as the presence of prostatic cysts were determined. Linear regression and correlation analysis were performed between prostatic parameters (length, width, height on sagittal and transverse images, and estimated volume) and parameters related to body size (body weight, body height, left kidney length and aortic diameter) and age of the dogs. Significant positive correlations were found between all prostatic parameters and parameters related to body size and age. Maximum predicted values for prostatic parameters for a given body weight and age were determined based on the upper limit of the 95% confidence interval of the mean predicted values. Such values should represent a useful tool for ultrasonographic evaluation of the prostate in the dog. Prostatic cysts were found in 14% of the dogs.

Stapled 1-stage functional end-to-end anastomosis and resection is a fast and safe procedure in the hand of nonexpert but trained surgeons.

Overexpression of the ERBB2 oncogene is observed in about 30% of breast cancers and is generally correlated with a poor prognosis. Previous results from our and other laboratories indicated that elevated transcriptional activity contributes significantly to the overexpression of ERBB2 mRNA in mammary adenocarcinoma cell lines. Activator protein 2 (AP-2) transcription factors account for this overexpression through two recognition sequences located 215 and 500 bp upstream from the transcription start site. Furthermore, AP-2 transcription factors are highly expressed in cancer cell lines overexpressing ERBB2. In this report, we examined the cooperative effect of Yin Yang 1 (YY1) on AP-2-induced activation of ERBB2 promoter activity. We detected high levels of YY1 transcription factor in mammary cancer cell lines. Notably, we showed that YY1 enhances AP-2␣ transcriptional activation of the ERBB2 promoter through an AP-2 site both in HepG2 and in HCT116 cells, whereas a carboxyl-terminal-truncated form of YY1 cannot. Moreover, we demonstrated the interaction between endogenous AP-2 and YY1 factors in the BT-474 mammary adenocarcinoma cell line. In addition, inhibition of endogenous YY1 protein by an antisense decreased the transcription of an AP-2-responsive ERBB2 reporter plasmid in BT-474 breast cancer cells. Finally, we detected in vivo AP-2 and YY1 occupancy of the ERBB2 proximal promoter in chromatin immunoprecipitation assays. Our data thus provide evidence that YY1 cooperates with AP-2 to stimulate ERBB2 promoter activity through the AP-2 binding sites.The ERBB2 proto-oncogene belongs to the epidermal growth factor receptor gene family and encodes a 185-kDa receptor tyrosine kinase (1). The ERBB2 gene is overexpressed in several human tumors, mostly in breast and ovary carcinomas where the overexpression is a marker of a poor prognosis (2).