A 54 year old man was referred to the department of neurosurgery for frontal headache and vomiting. The patient was known in the department because of previous multiple surgery for a locally invasive pituitary prolactinoma (eight years, three years, and one year previously). The neurological examination revealed a frontal mass, which adhered to the dura, suggesting a meningioma. One year later, a left temporal metastasis was removed. Three months later, the patient died, with spinal metastases, of massive lung embolism. Histology revealed a progression of adenohypophyseal prolactinoma on neuroendocrine carcinoma, with an increase in proliferating indexes and modification of hormone production. This study documents a 10 year history of a rare prolactin producing pituitary carcinoma, which metastasised via liquoral flow.
Seventy-six specimens of normal breast tissue and benign and malignant breast lesions were studied to assess the mean area occupied by silver-stained proteins of the nucleolar organizer regions (MNORA) of the nucleolus. The assessment was performed with a computer-assisted image analyzer. The results indicate that only 30% of malignant lesions have a MNORA value greater than that of normal breast tissue or benign lesions. On the other hand, MNORA values of ductal carcinoma in situ were significantly greater than those of epitheliosis (papillomatosis). MNORA values were also significantly different in grade I and grade III invasive ductal carcinomas, the latter exhibiting the highest MNORA values of all the cases observed. Evaluation of MNORA values may therefore help in differentiating benign epithelial proliferations from ductal carcinomas in situ. Furthermore, because there is evidence that MNORA values are indicative of the cell duplication rate, MNORA values may ultimately be considered an objective prognostic parameter in addition to grading for invasive ductal carcinomas.
Several studies performed at light microscopic level on cy-A qualitative and quantitative analysis of silvertohistological samples silver-stained for AgNOR proteins stained nuclear organizer regions (AgNOR) proteins was have shown that the quantity of these proteins progressively performed during hepatocarcinogenesis induced in rats increases when the cells enter the mitotic cycle from G1 to initiated by diethylnitrosamine (DENA) using the resisthe end of S-phase. 4,5 There is also evidence that the AgNOR tant-hepatocyte model. Nuclear proteins from control protein amount is directly related to the rapidity of cell duplihepatocytes, hyperplastic nodules, and hepatocellular cation in continuously dividing cells. synthesis of individual AgNOR proteins, butThe aim of the present work has been to study both the to an increased synthesis of nucleolin and protein B23, quantitative and the qualitative changes of individual Agwhich is associated with a progressive increased hepato-NOR proteins during liver carcinogenesis induced by the recyte proliferation rate. (HEPATOLOGY 1996;24:1269-1273.) sistant-hepatocyte model 19 in F-344 rats initiated by diethylnitrosamine (DENA). For this purpose, control hepatocytes, The silver-stained nucleolar organizer region (AgNOR) pro-hyperplastic nodules, and hepatocellular carcinomas (HCCs) teins are a group of proteins that are associated with the were used. The study was extended to human cirrhotic livers nucleolar organizer regions and are selectively stained by and HCCs. Western blots of nucleolar proteins were silversilver methods.1 During interphase, they are located in the stained specifically for AgNOR proteins 11 and the distribufibrillar nucleolar components.2 The AgNOR proteins are nec-tion of the silver-stained bands was examined. Quantification essary for ribosomal RNA transcription. 3 of individual AgNOR proteins was performed by densitometric analysis of silver-stained bands. MATERIALS AND METHODSAbbreviations: AgNORs, silver-stained nucleolar organizer regions; DENA, diethylnitroAnimals. Male Fisher rats (130-140 g at the beginning of the exsamine; HCC, hepatocellular carcinoma; BrdU, bromodeoxyuridine; LI, labeling index. periment) were purchased from Charles River (Milano, Italy). The Received April 19, 1996; accepted July 12, 1996. (200 mg/kg in 0.9% NaHCl, Sigma Chemical Co., St. Louis, MO).Supported by grants from Ministero della Ricerca Scientifica e Tecnologica (MURST)Two weeks after DENA administration, rats were subjected to a of the promotion regimen. Five animals that were subjected to a
Central nervous system involvement by Mycoplasma pneumoniae I read the article by Fink et al' with interest. I am surprised that their study population did not, except for a single case of Guillain-Barre syndrome, include patients with encephalitis, which is considered to be the main type of the central nervous system (CNS) involvement by Mycoplasma pneumoniae in children,2 despite the fact that their subjects were mainly children. When discussing CNS involvement by M pneumoniae, particularly in children, it is vital that patients with encephalitic episodes are examined as well. Recently, my research group studied CNS involvement by M pneumoniae using the polymerase chain reaction (PCR),3 and found that patients with encephalitis, in whom onset of neurological symptoms occurred within seven days of the onset of fever, exhibited a significantly higher incidence of mycoplasma DNA in cerebrospinal fluid (CSF) than patients with later onset of fever.4 Fink et al stated that six of seven patients with confirmed M pneumoniae infection reported a febrile illness or upper respiratory tract infection six to 14 days before the onset of neurological symptoms. Our data suggest that in most, but by no means all, of their patients mycoplasma DNA may not be detectable in the CSF. We are of the opinion that the presence of mycoplasma DNA in CSF is not evidence of a direct, invasive mechanism. Nevertheless, the clinical characteristics of illnesses involving the CNS or other factors, such as the interval between the onset offever and the onset ofthe neurological symptoms, should be taken into account before a conclusion is reached whether or not a direct invasive mechanism plays a role in CNS involvement by M pneumoniae.
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