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Biomedical subjects

R Stein-Werblowsky

Publications and source records attributed to R Stein-Werblowsky.

At least 19 recordsLinked to original sources
PubMed1997

Sexual behaviour and increased anal cancer.

An increase in epidermoid anal cancer has been observed in the past 30 years (1959-89). This increase in anal cancer has been noted to be more pronounced in women than men. The absence of a significant interactive effect of the HIV and human papillomaviruses and the incidence of anal cancer has been noted in some studies. These observations provide the rationale for consideration of other aetiologic agents that may contribute to the increase of anal cancer in men and women. Within the context of their ability to serve as cancer initiating and promoting factors, spermatozoa and seminal plasma are suggested as aetiologic agents and/or cofactors which are common to men and women practising anal intercourse in whom an increase in anal cancer has been observed. It is further suggested that sexual behaviour, that is, anal intercourse, not sexual preference, is one of the primary factors in the development of anal cancer.

Anus Neoplasms↗
PubMed1994

Sperm-induced urolithiasis in the rat.

Experiments are described demonstrating that experimental insemination with autologous or homologous sperm into the ventral prostate or bladder neck of outbred Zbar male rats induces intravesical precipitation or stones. These observations suggest that clinical conditions resulting in intravesical sperm may be contributory to bladder lithiasis in man and may have relevance to its prevalence in men vs. women.

Animals↗
PubMed1991

The persisting enigma of AIDS-associated Kaposi's sarcoma: a hypothesis.

The widespread prevalence of Kaposi's sarcoma during the HIV/AIDS epidemic and its unique epidemiological predilection for select groups 'at risk' for AIDS relative to their 'life-style' orientation provide the rationale for etiologic agent(s) other than HIV. In keeping with the requisites for the development and progression of malignancy, i.e., the transformation of normal to aberrant cells and the failure of host defenses to control them, is the rationale, in view of their respective properties, for the hypothesized participation of spermatozoa and/or seminal fluid components as being contributory to the development of Kaposi's sarcoma.

Acquired Immunodeficiency Syndrome↗
PubMed1983

The haematogenous spread of tumor: a prevental process.

The establishment of a secondary tumor is the outcome of a series of biological events. Cells detach from the primary tumor and penetrate vascular channels, which they leave again at a distant site to implant and proliferate in an organ or tissue remote from the primary tumor. These processes depend on the adhesion of tumor cells to each other, on the permeability of the venous or lymphatic channels and on the susceptibility of the substrate. Present experiments show that these properties are modifiable and that haematogenous tumor dissemination is a preventable process.

Animals↗
PubMed1981

On the retention of the fetus as a homograft.

The conceptus is tolerated in spite of the antigenic dissimilarities between mother and fetus. A new hypothesis to account for this phenomenon is put forward. It is suggested that the vessels within the trophoblastic villi--analogous to the vessels of malignant tumors--are permeable to humoral substances but impervious to cellular elements. This property allows for the exchange of nutrients and metabolites but, at the same time, precludes the passage of leukocytes. The block to diapedesis is believed to be due to the deposition of an occlusive layer of alpha 2-macroglobulin on vascular endothelium. The source of this protide is the fetal liver. In the absence of diapedesis there is no homograft reaction within the placenta. The "graft" is tolerated.

Animals↗
PubMed1980

On the prevention of haematogenous tumour metastasis to liver and lung.

Vascular endothelium is lined by a layer of alpha, 2, macroglobulin (AMG). This protide is believed to regulate the rate of extravasation of tumor cells. Experiments are described which show that increasing the deposition of AMG (enhancing its production and blocking its lysis) reduces the incidence of tumour metastases to liver and lung.

Animals↗
PubMed1980

A permeability-enhancing factor produced by tumor. The genesis of malignant effusions.

The intra-articular injection of ascites fluid or of extracts derived from malignant tumors was shown to induce exudative joint lesions. The intra-articular injection of normal plasma did not have this effect. It is suggested that tumor secretes a permeability-enhancing agent. This substance promotes the extravasation of humoral or cellular elements into the joint spaces. A similar mechanism may underlie the development of pulmonary arthropathy or the formation of malignant effusions.

Animals↗
PubMed1980

On the prevention of haematogenous tumor metastases rats. The role of the proteinase inhibitor "Trasylol".

All malignant tumors shed cells into the circulation. The number of circulating tumor cells bears no relation to the extent of secondary growth. This is determined by the number of tumor cells that cross the vessel wall and implant in extravascular sites. The rate of cellular emigration is regulated by the permeability of vessels harbouring tumor emboli, permeability in turn being dependent on the amount of alpha, 2, macro-globulin (AMG) lining vascular endothelium. Agents which inactivate or digest AMG, e.g. proteases, have been shown to promote the dissemination of tumor. Some tumors secrete large amounts of proteases. These enzymes are believed to lyse the AMG layer and so to facilitate the emigration of tumor cells. On this hypothesis, inhibitors of such proteases would have anti-metastatic properties. Present experiments lend support to this view. The proteinase inhibitor Trasylol, when allowed to act on tumor cells, has been shown to impair their capacity of setting up haematogenous metastases. It does not affect their viability or transplantability. It is suggested therefore, that blood-borne tumor dissemination might be inhibited by perfusing the (primary) tumor bed with proteinase inhibitor, possibly in association with AMG.

Animals↗
PubMed1978

On the lymphatic spread of cancer.

Experimental demonstration that agents promoting cellular motility and/or vascular permeability enhance the spread of tumour to regional or distant lymph nodes. Tumour emboli appear to reach the regional glands via the lymphatic channels and the distant nodes by haematogenous route.

Animals↗
PubMed1978

Vascular permeability in malignant disease.

Experimental demonstration that vessels draining large tumours are impermeable to cellular elements. Thus the pulmonary vessels of animals bearing large, primary (other than gastro-intestinal) cancers can become impermeable to tumour emboli. This imperviousness prevents the establishment of secondaries in the lung and promotes the transpulmonary passage of tumor cells. This phenomenon may account for the development of paradoxical metastases.

Animals↗
PubMed1978

On the latency of tumour cells.

The present experiments demonstrate that animals carrying large peripheral intramuscular tumours were free of spontaneous pulmonary metastases. Secondaries in the lung emerged, however, after administration of agents such as trypsin, 10% dextrose or antiserum to alpha-2-macroglobulin (AMG). Such metastases also appeared in animals treated with trypsin after amputation of the tumour-bearing limb. It is believed that the pulmonary vessels of tumour-bearing animals are lined with a layer of tumour-associated AMG. The presence of this peptide on vascular endothelium blocks the transmigration of tumour cells. Tumour emboli may remain dormant, i.e. unattached, in the vascular lumen. Agents inactivating AMG or enhancing vascular permeability (proteases, antisera to AMG or vasodilators) may promote the emergence of a latent tumour cell into an overt state. This is confirmed by the above experiments and by the microscopic appearance of the pulmonary vessels of test animals (shift of tumour cells from the intravascular to the perivascular space). It is suggested that latency is determined by the state of permeability of the vessels harbouring tumour emboli.

Animals↗