The cytologic criteria of synovial sarcoma in fine-needle aspirates were defined by a retrospective examination of 37 primary tumors. Irrespective of subtype, a typical pattern at low power was found, provided the yield was rich. The typical pattern was a mixture of dispersed cells with the presence of striped nuclei and cell-tight tumor tissue fragments with irregular borders. Often a branching network of vessels was present in the fragments, imitating a true vascular tumor. Except in poorly differentiated synovial sarcomas, the tumor cells were, small to medium in size, with rounded, ovoid, or fusiform bland nuclei with inconspicuous nucleoli. In the biphasic variant, small glandular- or acinar-like structures were present, although not in all cases. In the poorly differentiated type, however, the cellular pleomorphism was marked with the presence of cells with irregular nuclei and rhabdomyoblast-like cells, corresponding to the pleomorphic variant. The Ewing's sarcoma-like and the atypical spindle cell variants of poorly differentiated synovial sarcoma were not diagnosed in the material. An unequivocal diagnosis of sarcoma is possible when the yield is rich. However, ancillary diagnostics are necessary for a correct diagnosis, to avoid important pitfalls, such as other sarcomas with bland tumor cells and vessel-rich tumor fragments, in particular, solitary fibrous tumor and true hemangiopericytoma. Electron microscopic and/or molecular genetic analyses were better diagnostic adjuncts than immunocytochemistry.

Leptin, protein product of the ob gene, not only regulates food intake and energy expenditure but also has a number of other actions in the body. Leptin actions are mediated by its receptors that have either a long or a truncated intracellular domain, which is coupled to signal transduction pathways. Previous studies have demonstrated that human placenta expresses both leptin and its receptors. However, it is not known whether human umbilical cord and fetal membranes are also sites of expression of these molecules. Therefore, the present study investigated leptin and its receptor expression in these tissues from term pregnancy. Reverse-transcription polymerase chain reaction (RT-PCR) amplified expected size fragments of leptin and also its short and long receptor isoforms from umbilical cord and fetal membranes. The authenticity of PCR-amplified fragments was confirmed by Southern blot hybridization with corresponding cDNA probes. Western blotting revealed that the transcripts were translated into 16-kDa leptin, and 125-kDa (long) and 100-kDa (short) leptin receptor isoforms. However, the long form is present in umbilical cord and the short form in the fetal membranes. Immunocytochemistry revealed that leptin and its receptor isoforms were present in endothelial cells and smooth muscle of umbilical veins and artery, myofibroblasts in Wharton's jelly, amnion covering the cord, amnion and chorion in reflected fetal membranes and decidua from membranes. Amnion, however, contained the highest levels of leptin and its receptor immunostaining. In summary, term pregnancy human umbilical cord and fetal membranes co-express leptin and its receptor genes, which supports the hypothesis that leptin is an autocrine and paracrine regulator in these tissues.

Leptin, protein product of the ob gene, not only regulates food intake and energy expenditure but also has a number of other actions in the body. Leptin actions are mediated by its receptors that have either a long or a truncated intracellular domain, which is coupled to signal transduction pathways. Previous studies have demonstrated that human placenta expresses both leptin and its receptors. However, it is not known whether human umbilical cord and fetal membranes are also sites of expression of these molecules. Therefore, the present study investigated leptin and its receptor expression in these tissues from term pregnancy. Reverse-transcription polymerase chain reaction (RT-PCR) amplified expected size fragments of leptin and also its short and long receptor isoforms from umbilical cord and fetal membranes. The authenticity of PCR-amplified fragments was confirmed by Southern blot hybridization with corresponding cDNA probes. Western blotting revealed that the transcripts were translated into 16-kDa leptin, and 125-kDa (long) and 100-kDa (short) leptin receptor isoforms. However, the long form is present in umbilical cord and the short form in the fetal membranes. Immunocytochemistry revealed that leptin and its receptor isoforms were present in endothelial cells and smooth muscle of umbilical veins and artery, myofibroblasts in Wharton's jelly, amnion covering the cord, amnion and chorion in reflected fetal membranes and decidua from membranes. Amnion, however, contained the highest levels of leptin and its receptor immunostaining. In summary, term pregnancy human umbilical cord and fetal membranes co-express leptin and its receptor genes, which supports the hypothesis that leptin is an autocrine and paracrine regulator in these tissues.

In both SGA and AGA fetuses, glucose was mobilized during acidemia; lactate was higher in SGA at both a normal and low pH. Considering SGA being a proxy for fetal growth restriction, and acidemia a proxy for hypoxia, it is concluded that growth-restricted fetuses have an intact ability to develop lacticemia during hypoxia.

No abstract

Running foot: Effect of paracetamol on temperature in labour Wilcoxon matched-pairs signed-ranks test and cross-sectional data with Mann-Whitney U test. Shapes of the temperature curves were compared with mixed-effect models statistics for repeated measurements. The main outcome measures were temperature changes after paracetamol. A two-tailed P <0.05 was considered significant. RESULTS:Prior to T0 maternal and fetal temperatures increased in the paracetamol group, but after T0 no significant changes (P ≥0.1) were seen when compared with Wilcoxon signedranks test. In the control group, both temperatures increased from T-60 and onwards. Deltatemperatures (fetal minus maternal temperature) remained unchanged in both groups. The mixed-effect models analyses showed a significant difference (P =0.01) in the shape of fetal temperature curves between the paracetamol and control groups, but no significant difference (P =0.4) in maternal temperature curve shapes.