Objective To explore the clinicopathological features and diagnosis of adenoid cystic carci noma of the breast (ACCB).Methods Clinical data of 3 cases of ACCB were collected and followed up to observe the clinical pathological features.Immunohistochemistry was used to determine the immune phenotype.Results All the 3 cases were female,aging from 55 to 72 years old (61 years old as the average).The tumors were found in subareolar region well-circumscribed.ACCB was characterized by the presence of a dual cell population of luminal and basaloid cells arranged in cribriform and tubular-trabecular patterns.On immunohistochemical staining,the myoepithelial cells expressed SMA,CK5/6,P63,CD117 and the glandular epithelium cells were mostly positive for CK18,EMA,CK7,while no expression of ER,PR,HER-2,CD10 was observed.Conclusions ACCB is a rare neoplasm with a triple-negative,basal-like phenotype,but exhibits an indolent clinical behavior.The diagnosis can be worked out by evaluation of clinical characterstics,histological and immunohistochemical features.

Objective:To better understand the pathogenesis of obstructive jaundice (O J),a variety of rat OJ and biliary drainage models have been tried;however,complications are still common.We aimed to establish a stable rat model of OJ using microsurgical techniques,and to assess its reversal by internal bile drainage(IBD).Methods:After the pilot study,we developed a standardized surgical procedure.All operations were carried out under an operating microscope.In the first laparotomy,the proximal common bile duct (CBD) of the rat was ligated and transected.A tube was introduced into the distal end of the duct,and the other end of the tube was sealed and fixed.In the second laparotomy,the drainage tube was inserted into the (by now markedly dilated) proximal CBD,and ligated into position.We evaluated the general condition of the rats,the status of the liver and pancreas before and after IBD.Results:Complications such as intestinal reflux and bile duct blockage,were not found.Pancreatic injury was not evident by day 4 after the first laparotomy.After biliary drainage,the serum glucose and albumin concentration rapidly returned to normal levels.Liver weight/body weight ratio increased.The biochemical indicators and ultrasonographic elastography results for the liver gradually returned to normal.Conclusion:Using microsurgical techniques,we have developed a stable rat model of OJ reversed by IBD.

Mutations or inactivation of parkin, an E3 ubiquitin ligase, are associated with familial form or sporadic Parkinson's disease (PD), respectively, which manifested with the selective vulnerability of neuronal cells in substantia nigra (SN) and striatum (STR) regions. However, the underlying molecular mechanism linking parkin with the etiology of PD remains elusive. Here we report that p62, a critical regulator for protein quality control, inclusion body formation, selective autophagy and diverse signaling pathways, is a new substrate of parkin. P62 levels were increased in the SN and STR regions, but not in other brain regions in parkin knockout mice. Parkin directly interacts with and ubiquitinates p62 at the K13 to promote proteasomal degradation of p62 even in the absence of ATG5. Pathogenic mutations, knockdown of parkin or mutation of p62 at K13 prevented the degradation of p62. We further showed that parkin deficiency mice have pronounced loss of tyrosine hydroxylase positive neurons and have worse performance in motor test when treated with 6-hydroxydopamine hydrochloride in aged mice. These results suggest that, in addition to their critical role in regulating autophagy, p62 are subjected to parkin mediated proteasomal degradation and implicate that the dysregulation of parkin/p62 axis may involve in the selective vulnerability of neuronal cells during the onset of PD pathogenesis.
Adaptor Proteins, Signal Transducing ; chemistry ; metabolism ; Animals ; HEK293 Cells ; Heat-Shock Proteins ; chemistry ; metabolism ; Humans ; Lysine ; metabolism ; Mice ; Neurons ; metabolism ; pathology ; Oxidopamine ; pharmacology ; Parkinson Disease ; metabolism ; pathology ; Proteasome Endopeptidase Complex ; metabolism ; Protein Stability ; Proteolysis ; drug effects ; Sequestosome-1 Protein ; Ubiquitin-Protein Ligases ; metabolism ; Ubiquitination ; drug effects