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Trisomy 7, trisomy 10 and loss of the Y chromosome have been found by some authors in presumptive normal parts of human kidneys. We describe cytogenetic findings in short-term cultures from 58 biopsies obtained from non-neoplastic and neoplastic (renal cell carcinoma, RCC) tissues from the same kidney, the same types of tissues from independent kidneys, and tissue from kidneys without neoplasia. The results indicate the following. Non-neoplastic tissue from kidneys involved in RCC have (in mosaics) trisomies 5, 7, 10, 18 and loss of the Y as non-random clonal changes. They are not the result of local metastasis but are also found in kidneys with non-tumoral chronic pathologies and should thus not be considered specific for RCC. They are neither culturing artefacts nor a general phenomenon found in cultured normal solid tissues, but are acquired abnormalities, possibily related to various reactive cellular states in the tissues that are histologically normal. [ABSTRACT FROM AUTHOR]

Cytogenetic analysis of primary cell cultures from human atherosclerotic fibrous plaques revealed clonal chromosome abnormalities in 13 of the 18 cases studied. Loss of the Y chromosome and del(13)(q14) were present as single clonal abnormalities in eight cases; in five cases separate clones were found involving loss of the Y and a XXY karyotype, trisomy 10 and 18, loss of the Y and trisomy 7. A variety of single numerical and structural abnormalities were present in all but two of the 18 cases. Immunocytochemical studies were performed on cells from the same cultures used for cytogenetic analysis using monoclonal antibodies to human leucocyte common antigen, to human vimentin and to muscle actin. The immunoreactivity was positive for actin in 70-80% of the cells; 100% of the cells were positive for vimentin and all cells were ALC negative. These results indicated that the chromosomal abnormalities are present in the smooth muscle cells of the plaque. The hypothesis is proposed that the proliferation leading to the atherosclerotic lesion may primarily represent a hyperplastic response to mechanical and biological injuries and that this reactive proliferation is, in turn, associated with a tendency to chromosome instability. [ABSTRACT FROM AUTHOR]

Torsion of the adnexa has traditionally been treated by adnexectomy because of the fear of emboli departing from thrombosed ovarian veins. Several recent reports have described successful conservative management with unwinding of the twisted adnexa. As the trend toward conservative management progresses, the incidence of recurrent adnexal torsion may increase. We present a case of a 33 year old gravida 3, para 2 Caucasian female who presented at 7 weeks gestation complaining of symptoms similar to those experienced during an episode of right ovarian torsion treated by laparoscopic unwinding 6 years earlier. Colour Doppler sonography revealed absent flow in the right adnexa. The twisted right adnexa containing the presumed corpus luteum of pregnancy was laparoscopically unwound. Using an extracorporeal suturing technique, a laparoscopic oophoropexy was performed to prevent any further rotatory movement. This appears to be the first reported case of laparoscopic oophoropexy for a recurrent ovarian torsion; we encourage the use of this simple, minimally invasive procedure in cases of recurrent adnexal torsion. [ABSTRACT FROM AUTHOR]