Biomedicine International Journals
Volume:4 Issue: 2, 2013

Bacillus Calmette-Guérin (BCG) is currently the standard therapy for treating high grade non-invasive bladder cancer. BCG is superior to intravesical chemotherapy. The antitumor effect of BCG seems to be related to cellular immunological mechanisms. However, its precise mode of action is unknown. High-risk non-invasive bladder tumors in patients will progress to muscle-invasive bladder cancer despite BCG treatment. Traditional prognostic factors are mainly based on histopathological characteristics. However, there are no clear definitive markers for the response to therapy, partly because of a lack of knowledge concerning the mechanism of action utilized by BCG to mediate the observed clinical response. In response to the inflammatory process, the urothelial and tumor cells upregulate the expression of important surface proteins, such as major histocompatibility antigens, adhesion molecules, and death receptors. These proteins might serve as markers and potential therapeutic targets to enhance BCG efficacy. The genetic and molecular changes that occur in transitional cell carcinoma (TCC) of the bladder are numerous. Recent advances in carcinogenesis research will permit the discovery of new markers in patients treated with BCG that are directly involved in the pathogenesis of bladder cancer. Further investigations of the antitumor effect of intravesical BCG will lead not only to a potential enhancement of the BCG response, but probably also to a better understanding of bladder carcinogenesis.

A series of infectious-like events are characterised within the geographical area of the Scottish NHS Health Boards. Each event leads to a relatively sudden 3% increase in total deaths (around 3,500 extra deaths for Scotland) which lasts for around two to three years. The onset and shape of the time trend is slightly different in each Health Board area and it is this which suggests an infectious spread. There is a general north to south movement in each outbreak with initiation always occurring in Scotland before England. The number of medical admissions and emergency department attendances also rise at roughly the same time as the onset of these events. A similar phenomena has been documented in Australia, Canada and the USA and the effects appear to extend to general practitioner (GP) referrals, occupied beds in hospitals, the trajectory of incidence for specific cancers and a cycle in the gender ratio at birth. The possibility that the ubiquitous immune modifying herpes virus, cytomegalovirus, may be involved in these events is discussed.

The condylar emissary vein traverses the condylar canal and connects the sigmoid sinus to the suboccipital venous plexus. Although the condylar emissary vein is a potential route for infection and metastasis, there exists a paucity of published studies on the anastomosis and histology of this vein. We present a variation observed during dissection of a 77-year-old, formalin-fixed female cadaver during a medical school anatomy course. Blunt and sharp dissections of the cervical spine, systematic measurements, histologic preparations of the vasculature, and a literature search were performed. The left condylar emissary vein directly connected the sigmoid sinus to the deep cervical vein with an additional anastomotic venous branch to the vertebral venous plexus. Histologic examination of the condylar emissary vein demonstrated arterialization of the vein with extensive elastic fibers permeating all layers. To our knowledge, this is the first study to describe the histology of the condylar emissary vein. Awareness of the histology of the condylar emissary vein and related extracranial anastomotic variations may be of use during neurosurgery of the suboccipital region. Furthermore, since the condylar emissary vein can serve as a route for metastatic spread of cancer, pathologists and radiologists couldalso benefit from awareness of its morphology.

Melanodacryorrhea, or black-colored tears, is an extremely rare condition. A review of the literature yields very few articles on its pathophysiology. The authors discuss three identified causes of melanodacryorrhea: uveal melanoma, ocular mycosis, and bilateral conjunctival argyrosis.