Notes: Abstract In repair of coarctation in neonates or young infants, inadequate removal of ductal tissue, failure to address hypoplasia of the aortic arch, and suture line tension have been reported to be important factors of residual or early recurrent stenosis at the coarctation repair site. In a consecutive series of neonates and young infants with coarctation, who were all operated without delay with extended resection, the clinical outcome regarding the development of restenosis and hypertension was studied. In addition, the resected specimens were investigated regarding the completeness of resection of ductal tissue. Twenty-five consecutive neonates and young infants (median age 22 days, range 5 to 39 days) who underwent surgical correction of coarctation were reviewed; the resected specimens were examined histologically to document the extent of ductal tissue in the aortic wall. Fifteen patients had a preductal coarctation with associated cardiovascular anomalies including a hypoplastic aortic arch (n = 11). The remaining 10 patients had a paraductal coarctation without associated intracardiac anomalies. In all patients, the isthmus was bypassed and an end-to-side anastomosis was constructed between the descending aorta and the undersurface of the proximal aortic arch (n = 13) or the distal ascending aorta (n = 12). In 13 patients without marked hypoplasia of tbe aortic arch, the coarctation repair was performed through a left thoracotomy. In the remaining 12 patients, the coarctation was repaired through a median sternotomy with CPB and hypothermic circulatory arrest, on the basis of an associated hypoplastic aortic arch (n = 4), hypoplastic aortic arch with intracardiac anomalies (n = 7), or a “bovine” innominate artery (n = 1). There was no perioperative or late mortality. At a median follow-up of 15 months, 1 patient (4%) developed a recurrent stenosis at the coarctation repair site; in the remaining 24 patients, echocardiograpby showed a widely patent anastomosis with no evidence of a hemodynamically significant gradient. None of the patients had hypertension. Histologic examination of the resected specimens demonstrated the presence of ductal tissue in the descending aorta with maximal extension into its lateral wall (mean 5.2 mm). In all specimens of the paraductal subtype, there was also extension of ductal tissue into the lateral wall of tbe isthmus (mean 3.9 mm). We conclude that: (1) in the absence of marked hypoplasia of the proximal aortic arch, coarctation can be repaired with low mortality and morbidity via a left thoracotomy; (2) in the presence of marked hypoplasia of the proximal aortic arch and/or if associated intracardiac defects also need to be repaired, we advocate repair of the coarctation and associated defects through a median sternotomy with circulatory arrest; (3) in view of the absence of postoperative hypertension in this series, early repair of aortic coarctation is recommended; and (4) because ductal tissue may extend not only into the descending aorta but also into the isthmus, complete excision of the coarctation and bypass of the isthmus are valuable techniques to avoid secondary constriction of the aorta by ductal tissue.

Notes: Abstract Tenascin (tenascin-C), a mesenchymal glycoprotein, is expressed in many tissue remodeling processes. We evaluated tenascin expression during androgen-deprivation-related involution of the rat prostate. At set intervals following castration and subsequent testosterone repletion, prostates were removed in 30 adult rats. Each prostate was immunostained with a polyclonal antiserum against rat tenascin and keratin antibodies specifically directed against exocrine basal cells and luminal cells in the prostate glandular structure. Morphologic impressions were semiquantatively evaluated using a computer-assisted image analysis system. Rat prostates showed a transient increase in the periglandular tenascin expression directly following castration that reached a maximum at day 3. At day 6, tenascin expression was similar to control prostates. This was accompanied by a decrease of cells in the luminal cell layer. The weakest tenascin immunoreactivity was noted on day 14 after androgen withdrawal. This process was reversed by androgen repletion. This study shows that in the rat prostate tenascin expression may be androgen dependent and that during androgen deprivation-related involution tenascin expression is probably associated with tissue remodeling by stromal-epithelial interactions.

Notes: Abstract  A selection of normal human tissues was investigated for the presence of lamins B1, B2, and A-type lamins, using a panel of antibodies specific for the individual lamin subtypes. By use of immunoprecipitation and two-dimensional immunoblotting techniques we demonstrated that these antibodies do not cross-react with other lamin subtypes and that a range of different phosphorylation isoforms is recognized by each antibody. The lamin B2 antibodies appeared to decorate the nuclear lamina in all tissues examined, except hepatocytes, in which very little lamin B2 expression was observed. In contrast to previous studies, which suggested the ubiquitous expression of lamin B1 in mammalian tissues, we show that lamin B1 is not as universally distributed throughout normal human tissues as was to be expected from previous studies. Muscle and connective tissues are negative, while in epithelial cells lamin B1 seemed to be preferentially detected in proliferating cells. These results correspond well with those obtained for lamin B1 in chicken tissues. The expression of A-type lamins is most prominent in well-differentiated epithelial cells. Relatively undifferentiated and proliferating cells in epithelia showed a clearly reduced expression of A-type lamins. Furthermore, most cells of neuroendocrine origin as well as most hematopoietic cells were negative for A-type lamin antibodies.