Quiescent Volcano—Chest Wall Hemangioma

Chest wall hemangiomas are rare tumors that may originate within the soft tissue or from the ribs. Intramuscular hemangioma is infrequent, representing less than 1 % of all hemangiomas, and the localization in the chest wall is even less frequent. They are typically cutaneous in location, large, and poorly circumscribed and can be locally destructive. We present a case of a 34-year-old lady presented with firm lump 3 × 3 cm in left upper and inner quadrant of left breast well defined borders, non-pulsatile and restricted mobility. Sono-mammogram was suggestive of ill-defined lesion at 10 o’clock position. CT chest was conclusive of chest wall hemangioma. The patient underwent excision of the lump. HPE was suggestive of cavernous hemangioma. Cavernous hemangioma typically manifest at birth or before the age of 30 years. CT is more sensitive than plain radiography in detecting phleboliths, which are present in approximately 30 % of cavernous hemangiomas. Surgical excision would be treatment of choice. In this case, the site of the lesion was in the breast clinically mimicking that of a fibroadenoma which warrants hemangioma as a differential diagnosis.     

Elevated Src family kinase activity stabilizes E-cadherin-based junctions and collective movement of head and neck squamous cell carcinomas

EGF receptor (EGFR) overexpression is thought to drive head and neck carcinogenesis however clinical responses to EGFR-targeting agents have been modest and alternate targets are actively sought to improve results. Src family kinases (SFKs), reported to act downstream of EGFR are among the alternative targets for which increased expression or activity in epithelial tumors is commonly associated to the dissolution of E-cadherin-based junctions and acquisition of a mesenchymal-like phenotype. Robust expression of total and activated Src was observed in advanced stage head and neck tumors (N=60) and in head and neck squamous cell carcinoma lines. In cultured cancer cells Src co-localized with E-cadherin in cell-cell junctions and its phosphorylation on Y419 was both constitutive and independent of EGFR activation. Selective inhibition of SFKs with SU6656 delocalized E-cadherin and disrupted cellular junctions without affecting E-cadherin expression and this effect was phenocopied by knockdown of Src or Yes. These findings reveal an EGFR-independent role for SFKs in the maintenance of intercellular junctions, which likely contributes to the cohesive invasion E-cadherin-positive cells in advanced tumors. Further, they highlight the need for a deeper comprehension of molecular pathways that drive collective cell invasion, in absence of mesenchymal transition, in order to combat tumor spread.     

A High Proliferation Rate is Critical for Reproducible and Standardized Embryoid Body Formation from Laminin-521-Based Human Pluripotent Stem Cell Cultures

When aiming for homogenous embryoid body (EB) differentiation, the use of equal-sized EBs is required to avoid a size-induced differentiation bias. In this study we developed an efficient and standardized EB formation protocol for human pluripotent stem cells (hPSC) cultured in a laminin-521-based xeno-free system. As the cell proliferation rate of the cells growing on laminin-521 strongly affected the efficiency of aggregate formation, we found that recently passaged cells, as well as the addition of ROCK inhibitor, were essential for reproducible EB formation from hPSC single-cell suspensions. EBs could be obtained in a variety of differentiation media, in 96-well round-bottom plates and in hanging drops. Gene expression studies on differentially sized EBs from three individual human embryonic stem cell lines demonstrated that the medium used for differentiation influenced the differentiation outcome to a much greater extent than the number of cells used for the initial EB formation. Our findings give a new insight into factors that influence the EB formation and differentiation process. This optimized method allows us to easily manipulate EB formation and provide an excellent starting point for downstream EB-based differentiation protocols.     

Myoklonus – eine Orientierungshilfe

The puzzling variety of myoclonus is a diagnostic and therapeutic challenge. Early in the diagnostic work-up of myoclonus, electrophysiologic investigations should clarify whether it is myoclonus or not, and whether there are topographic clues, clinical or electrophysiological, to the generating structure. Such clues would influence both the laboratory strategies or neuroimaging investigations aimed at the underlying disease and the selection of drugs to suppress myoclonus.     

Synkopen

Syncope occurs in approximately 25% of the population at least once during their lifetime. It therefore represents the most frequent differential diagnosis of an epileptic seizure. Depending on the prognosis and therapy, syncopes can be divided in cardiac syncope, syncope due to orthostatic hypotension and reflex syncope, of which vasovagal (neurocardiogenic) syncope is the most frequent type. Vasovagal syncope typically occurs after prolonged standing, the sight of blood, pain and medical procedures. The pathophysiology is not well understood. Genetic factors play a role as well, mainly following a complex mode of inheritance. Syncope can usually be differentiated from an epileptic seizure based on the medical history. Typical vasovagal triggers, a typical prodrome and pallor suggest syncope, whereas cyanosis, tongue biting and a prolonged postictal state favor an epileptic seizure. In cases of doubt or if cardiac syncope is suspected additional diagnostic tests may be necessary. Due to the increased mortality, patients with cardiac syncope need urgent cardiological treatment. The aim of the treatment of vasovagal syncope is to avoid additional events as this type is not associated with increased mortality. This can be achieved by behavioral changes, e.g. avoiding the trigger situation and lying down or tensing of arm and leg musculature during the prodrome to avoid further reduction of blood pressure. There is only sparse evidence for pharmacotherapeutic options. Cardiac pacemakers mostly have no effect. The implantation of a pacemaker seems to be beneficial only in patients over 40 years old with frequent vasovagal syncope, asystole and negative tilt table test.