Cell proliferation and death: morphological evidence during corticogenesis in the developing human brain.

Cell proliferation and death account for the refinement of the cell number during corticogenesis. These processes have been investigated in the human developing telencephalon (12th-24th week of gestation) and cerebellum (16th-24th week). Only foetal brains, which had normal neuropathological examination, were utilised. Cell proliferation was analysed by classical histology and PCNA immunohistochemistry; cell death was investigated by the TUNEL method, which makes evident the different stages of apoptosis. High figures of mitotic nuclei were seen in the ventricular zone at the 12th-15th week of gestation, before sharply declining. The decrease of the proliferating cells occurs synchronously in both frontal and occipital germinal zones. Conversely, a slow increase of the number of the mitotic cells was observed in the more dorsal regions, probably due to the presence of proliferating glial elements. The amount of apoptotic nuclei was always remarkably low in the transient compartments of the wall of the telencephalon. The moderate number of apoptotic cells suggests that cellular mechanisms other than apoptosis are involved in the dissolution of the ventricular zone. Neither proliferating nor apoptotic cells were seen in the cortical plate. The topography of cell proliferation and death in the developing cerebellum did not account for a mutual relationship between the two events. The prolonged duration of the cell-cycle in the human developing CNS may explain its increased vulnerability to various DNA-damaging conditions, which can lead to either destructive lesions or malformations.

Bladder endometriosis: deep infiltrating endometriosis or adenomyosis?

OBJECTIVE: To describe the anatomopathologic characteristics of endometriosis infiltrating the bladder detrusor. DESIGN: Descriptive anatomopathologic study. SETTING: Tertiary care center for endometriosis. PATIENT(S): Four patients, aged 22-38 years, who underwent laparotomy for bladder endometriosis. INTERVENTION(S): Surgical excision and pathologic analysis of bladder endometriotic nodules in four patients. MAIN OUTCOME MEASURE(S): Gross and microscopic characteristics of endometriotic nodules. RESULT(S): A nodule of adenomyosis on the anterior wall of the uterus, in continuity with the detrusor lesion, was excised in three patients. In the other patient, bladder endometriosis was continuous with a nodule that infiltrated the left parametrium and extended as far as the posterior leaf of the ipsilateral broad ligament. Microscopically, all of the lesions had a similar histologic pattern: foci of endometriosis scattered in the bladder wall. The main feature was the paucity of endometrial-type stroma, particularly in the bladder submucosa, where glands were almost always dilated and cystlike and were lined by flattened cells. CONCLUSION(S): Analysis of our patients, although it does not pinpoint the pathogenesis of the disease, seems to exclude the hypothesized intraperitoneal origin of endometriotic lesions of the bladder detrusor.

Differential expression of p57kip2, a maternally imprinted cdk inhibitor, in normal human placenta and gestational trophoblastic disease.

Evidence has recently been provided to support a role for genomic imprinting in the regulation of embryonic implantation and development and placental growth, as well as in the pathogenesis of proliferative trophoblastic diseases. The cyclin-dependent kinase inhibitor p57KIP2 has recently been recognized as a maternally imprinted gene. We investigated p57KIP2 expression in first-trimester normal placentas from interrupted pregnancy, spontaneous abortions, and different types of proliferative trophoblastic diseases using single- and double-marker immunohistochemical techniques. In normal placenta, nuclear p57KIP2 expression was observed at high frequency (up to 100%) in extravillous trophoblast, cytotrophoblast, and implantation-site interstitial trophoblast, but was absent in syncytiotrophoblast. p57KIP2 was also expressed in the stromal cells of maternal decidua, which was one of the few adult tissues retaining p57KIP2 expression (most other adult tissues investigated were negative). p57KIP2 expression was either absent or low in all cases of diploid/tetraploid complete moles (20 cases) and in three cases of gestational choriocarcinoma. On the other hand, all spontaneous abortions (12 cases) and triploid partial moles (19 cases) showed p57KIP2 levels comparable to those observed in normal placenta. These findings are in line with the hypothesis that deregulation of genomic imprinting, particularly the loss of cell-cycle inhibitors such as p57KIP2, is involved in the abnormal development of androgenetic trophoblastic proliferations. In addition, this simple immunohistochemical analysis could provide a useful diagnostic marker in difficult cases.

Genomic imprinting in human biology and pathology.

Evidence has been recently provided on the relevant role of genomic imprinting in the regulation of implantation, embryonic development, placental growth, and also in development of proliferative trophoblastic diseases and human carcinogenesis. Among the various imprinted genes the cyclin-dependent-kinase inhibitor p57KIP2 (maternally imprinted) is particularly interesting since it can function as a tumor suppressor gene. In this review we describe the different roles of genomic imprinting in human diseases, with particular emphasis on the role of p57KIP2 in molar pregnancy and in tumorigenesis.

Chronic hepatitis in multiple virus infection: histopathological evaluation.

The frequency and histological pattern of multiple hepatitis virus infection was studied in 161 Italian patients who had consecutively undergone liver biopsy from 1989 to 1991. The histological features were compared with that of infection with a single virus. Thirty-nine per cent of patients had evidence of past or present multiple infection, the commonest of which was hepatitis C virus (HCV) in patients with evidence of previous infection with hepatitis B virus (HBV). In general, the severity of the histological pattern of each viral infection was maintained even when more than one virus was involved; there was neither exacerbation nor diminution of the histological changes. The delta-virus (HDV) was not associated with severe necro-inflammatory lesions, but HDV-positive patients were few in this cohort. Lymphoid follicle formation (a putative histological marker of HCV infection) was also found in a high proportion of HCV-negative patients but expressing much HBcAg or HDAg in liver tissue. Possible explanations for this finding are that follicles are relatively non-specific for HCV infection, or that these cases represent HCV infection with false-negative serology. The results of this study suggest that multiple hepatitis virus infection is common in the population investigated and that HBV and HCV co-infection cannot be reliably diagnosed histologically. Whether double infection with these viruses influences the cirrhotic evolution of the liver lesion remains unclear.

Mediastinal chondrosarcoma. Case report.

A 34-year-old man and a 71-year-old woman underwent radical removal of mediastinally sited chondrosarcoma, presumably originating in the periosteum of the vertebral body. The man (with mesenchymal chondrosarcoma) died of remote metastasis 6 years postoperatively. The woman (poorly differentiated chondrosarcoma, grade 2-3) is still alive 2 years after the operation.

[Mesenchymoma of the mediastinum (a case report)]. / Il mesenchimoma del mediastino (presentazione di un caso).

A 44-year-old male affected by mesenchymoma of the mediastinum was treated surgically. The neoplasm, localized in the postero-inferior mediastinum with prevalent development to the left, was found to consist of adipose, leiomuscular and myxoid tissue. The patient was asymptomatic. Complete removal of the neoplasm proved possible, and one year after surgery no signs of recurrence were present. Few cases of mediastinal mesenchymoma have been reported.

Increased levels of soluble interleukin-2 receptor in non-Hodgkin's lymphomas. Relationship with clinical, histologic, and phenotypic features.

In this study the authors investigated the serum levels of the released soluble form of interleukin-2 receptor (sIL-2R) in patients with non-Hodgkin's lymphomas (NHLs). Data were evaluated in relationship to the morphologic and immunophenotypic heterogeneity of NHL at diagnosis and in progressive advanced diseases. Increased sIL-2R levels were found in most cases, when compared with levels observed in healthy controls. No obvious statistical correlation has been observed between sIL-2R values in different NHL subtypes as defined by current classifications. On the other hand, major significance was related to the extent of the disease. Very high values, comparable to those observed in hairy cell leukemia, were observed in a number of large cell NHLs complicating low-grade B-cell lymphoproliferations and in a single case of T-cell Kil+ NHL. The authors' findings suggest that the detection of sIL-2R in NHL may represent a good marker in improving risk assignment of single cases and/or for monitoring remissions and exacerbations during the treatment of cases with very high levels at diagnosis. Nevertheless, the observed overlap between groups on an individual case basis can render the clinical application of this marker problematic.

[A case of brown tumor of the vomer]. / Osservazione di un caso di tumore bruno del vomere.

A case of brown-tumor of the vomer in a 21-year-old woman is described. The term giant cell lesions encompasses a variety of conditions. Three distinct entities are found in the facial area i.e. giant cell reparative granuloma, true giant cell tumor and brown-tumor. After having described the clinical, radiological and histopathological characteristics of the lesion, emphasis is placed on the importance of clinical, anamnestic, laboratory, radiological and histological findings in accurately differentiating the various types of giant cell lesions of the facial skeleton.