bluuebunny/crossref_metadata_2025_split huggingface dataset:
Delayed appearance of decorin in healing burn scars
Authors: Sayani  , Dodd  , Nedelec  , Shen  , Ghahary  , Tredget  , Scott  
Published: March 2003

AimsWe have previously shown that hypertrophic scar tissue from burn patients contains abnormally high amounts of the proteoglycans versican and biglycan and reduced amounts of decorin, in comparison with normal dermis or mature scar. The lack of decorin may account for the poor organization of collagen fibrils in the nodular areas of these scars. Decorin has also been reported to neutralize the fibrogenic growth factor TGF‐β1. This study was conducted to monitor the time‐course of expression of decorin in healing burn wounds by in‐situ hybridization to determine whether its absence from hypertrophic scars could result from reduced synthesis.Methods and resultsScar tissue from 19 patients and normal dermis from six patients, was fixed in paraformaldehyde, embedded in paraffin and sectioned. Digoxigenin‐labelled cRNA probes were prepared from a plasmid containing a 622‐bp insert of human decorin cDNA and used for in‐situ hybridization. Total numbers of connective tissue cells and cells positive for decorin mRNA were counted in 10 random fields in the upper (papillary), middle and lower (reticular) one‐thirds of the dermis. In all regions the number and percentages of cells with decorin mRNA were low during the first 12 months after injury (eight samples), much higher between 12 and 36 months (seven samples) and low and similar to those in normal skin after 36 months (five samples). The differences between intermediate and early or late stage samples were statistically significant (one‐way anova). Immunohistochemistry showed little staining for decorin in early stage samples and much stronger staining in mid‐stage. Late stage tissue showed intense staining for decorin, almost comparable to that in normal dermis.ConclusionExpression of decorin in burn wounds is suppressed for about 12 months and then increases at a time when resolution of hypertrophic scarring is generally considered to occur.
Expression of thyroid transcription factor‐1 in pulmonary and extrapulmonary small cell carcinomas and other neuroendocrine carcinomas of various primary sites
Authors: Kaufmann  , Dietel  
Published: March 2003

AimsThe thyroid transcription factor‐1 (TTF‐1) is a highly specific immunohistochemical marker for the identification of pulmonary adenocarcinomas and non‐neuroendocrine large cell carcinomas, especially in patients presenting with metastatic carcinomas of unknown primary site. In this study we tested if anti‐TTF‐1 can also be used to verify a pulmonary origin of neuroendocrine carcinomas, placing emphasis on the discrimination of pulmonary small cell carcinomas (SCCs) from extrapulmonary SCCs and the distinction of SCCs from Merkel cell carcinomas of the skin.Methods and resultsWe studied 37 pulmonary SCCs, 15 SCCs of extrapulmonary origin, 4 pulmonary large cell neuroendocrine carcinomas (LCNECs), four extrapulmonary LCNECs, six medullary thyroid carcinomas, 16 Merkel cell carcinomas, and a total of 32 carcinoids/low‐grade neuroendocrine carcinomas of pulmonary (12 cases) and extrapulmonary (20 cases) origin. Using the commercially available monoclonal antibody 8G7G3/1, TTF‐1 was immunohistochemically detectable in 81% of pulmonary SCCs but also in 80% of extrapulmonary SCCs. Furthermore, anti‐TTF‐1 showed a positive staining in 50% of all pulmonary carcinoids, in one gastric carcinoid, in 2/4 of pulmonary, and 1/4 of extrapulmonary LCNECs. All medullary thyroid carcinomas were also TTF‐1‐positive. Merkel cell carcinomas were consistently TTF‐1‐negative.ConclusionsOur results suggest that in contrast to non‐neuroendocrine carcinomas, anti‐TTF‐1 cannot be used to prove or to exclude a pulmonary origin of SCCs or LCNECs of unknown or uncertain primary site. Therefore, before using anti‐TTF‐1 as a marker for pulmonary carcinomas one should be sure to have excluded SCC and LCNEC. On the other hand, anti‐TTF‐1 might be used to specifically discriminate SCCs of various origin from Merkel cell carcinomas.
Polymorphous low‐grade adenocarcinoma and adenoid cystic carcinoma: distinct architectural composition revealed by collagen IV, laminin and their integrin ligands (α2β1 and α3β1)
Authors: Loducca S V L , Raitz R , S Araújo N , Araújo V C 
Published: March 2003

Aims:Polymorphous low‐grade adenocarcinoma (PLGA) and adenoid cystic carcinoma (ACC) are malignant salivary gland tumours bearing many similar histological patterns. This study was undertaken to show how the presence and distribution of collagen IV and laminin, and their ligands (integrin α2β1 and α3β1 components), can reveal histoarchitectural differences which distinguish these two entities.Methods and results:Five cases of ACC and five cases of PLGA from the archives of the Oral Pathology Department of the School of Dentistry of the São Paulo University were submitted to immunostaining with the antibodies to collagen IV, laminin, and integrins α2β1 and α3β1 using the streptavidin–biotin–peroxidase technique. Positive and negative controls were included. PLGA showed a thin line of collagen IV and laminin surrounding structures composed of a single cell layer. Integrins were expressed as a widespread and granular pattern. A thick line of collagen and laminin was observed around the neoplastic structures of ACC. Both integrins were expressed in intercellular spaces and around luminal spaces of tubular structures.Conclusions:Collagen IV and laminin, and their integrin ligands, are useful in demonstrating that neoplastic ductal units of PLGA are composed of a single cell layer, being distinct from ACC which contains structures composed of two layers of neoplastic cells.
Arteriolitis in renal transplant biopsies is associated with poor graft outcome
Authors: Bellamy C O C , Randhawa P S 
Published: March 2003

Aims: The Banff 1997 classification of renal allograft pathology identifies arteriolitis as a finding of uncertain significance. We sought to improve our understanding of arteriolitis by correlating its occurrence with histopathological and clinical parameters.Methods and resultsTwenty allograft kidney biopsies from 19 patients, showing arteriolitis, were identified. Arterioles were defined as small vessels with: (1) wall thickness of 1–3 myocytes; (2) diameter less than one‐third of an adjacent glomerulus; and (3) discontinuous or absent elastica. Arteriolitis was defined as mural infiltration by lymphocytes. Other histological findings were categorized according to the Banff 1997 working formulation. Ten biopsies (50%) showed type IIA rejection, seven (35%) showed type I rejection, and three (15%) showed borderline change. Two patients with borderline change had acute rejection in the next biopsy. None of the seven patients with type I rejection had previous or subsequent type II rejection on biopsy. A total 11/20 biopsies (10/19 patients) showing arteriolitis had type IIA rejection in the index or next biopsy. On follow‐up, graft loss due to rejection occurred in 5/19 (26%) patients (median 126 days); all had shown type IIA rejection on a previous biopsy. Chronic allograft nephropathy developed in a further 4/19 (21%) patients (median 157 days), of whom three had shown only type I rejection on biopsy.ConclusionArteriolitis is associated with acute rejection, often type II rejection, and is associated with poor graft outcome. Other causes of arteriolitis were not encountered in this series.
All infiltrating T‐lymphocytes in Hodgkin's disease express immunohistochemically detectable T‐cell receptor ζ‐chains in situ
Authors: Dukers D F , Oudejans J J , Jaspars E H , Gras M , Vos W , Middeldorp J M , Meijer C J L M , Bloemena E 
Published: March 2003

Aim: We studied the expression of TCR ζ‐chain on tumour‐infiltrating lymphocytes in EBV‐positive and EBV‐negative cases of Hodgkin's disease (HD), to assess whether downregulation of TCR ζ‐chain on tumour‐infiltrating lymphocytes might be a mechanism for immune escape of the neoplastic cells.Methods and resultsBy immunohistochemistry we investigated tissue of 27 cases of primary HD, both paraffin embedded and frozen, for the presence of T‐cell receptor complex ζ‐chain and other T‐cell markers on the reactive cells. Strong membranous staining of TCR ζ‐chain was present in all cases in frozen tissue. In contrast, in paraffin‐embedded material substantial loss of TCR ζ‐chain was detected in old (> 6 years) tissues. However, no differences in either the number of positive cells or their staining intensity were observed in EBV‐positive and negative cases of HD as detected in frozen tissue. Storage of paraffin‐embedded tissue leads to a rapid and substantial loss of TCR ζ‐chain reactivity compared to frozen material of the same HD cases. Staining reactivity of other T‐cell markers (CD3, CD4 and CD8) on paraffin‐embedded material remained unaffected. Immunofluorescent double‐staining confirmed colocalization and coexpression of TCR ζ‐chain and CD3.ConclusionsIn frozen biopsies of primary HD TCR ζ‐chain was expressed on all reactive CD3‐positive cells, both in EBV‐positive and EBV‐negative cases. This suggests that ζ‐chain downregulation is not a likely mechanism whereby neoplastic cells of HD can escape immune surveillance.
Distinction between coeliac disease and refractory sprue: a simple immunohistochemical method
Authors: Patey‐Mariaud de Serre N , Cellier C , Jabri B , Delabesse E , Verkarre V , Roche B , Lavergne A , Brière J , Mauvieux L , Leborgne M , Barbier J P , Modigliani R , Matuchansky C , Macintyre E , Cerf‐Bensussan N , Brousse N 
Published: March 2003

AimsWe recently showed that refractory sprue is distinct from coeliac disease, the former being characterized by abnormal intraepithelial T‐lymphocytes expressing a cytoplasmic CD3 chain (CD3c), lacking CD3 and CD8 surface expression, and showing TCRγ gene rearrangements. To take advantage of the abnormal phenotype of CD3c + CD8 − intraepithelial lymphocytes (IEL) in refractory sprue we developed a simple method to distinguish coeliac disease from refractory sprue.Methods and resultsComparative immunohistochemical studies using anti‐CD3 and anti‐CD8 antibodies were applied on paraffin‐embedded and frozen biopsy specimens in refractory sprue (n = 6), coeliac disease (n = 10), healthy controls (n = 5) and suspected refractory sprue (n = 6). Comparable results were obtained on fixed and frozen biopsy specimens. In four of the six patients with suspected refractory sprue, abnormal CD3c + CD8 − IEL and TCRγ gene rearrangements were found, as in refractory sprue; the remaining two patients had normal (CD3 + CD8 +) IEL and no TCRγ gene rearrangements. Both patients had coeliac disease, as one failed to comply with a gluten‐free diet, while the other was a slow responder.ConclusionThis simplified immunostaining method using anti‐CD3 and anti‐CD8 antibodies on paraffin sections can distinguish active coeliac disease from refractory sprue and should prove useful in clinical practice.
Bone marrow manifestations of infections and systemic diseases observed in bone marrow trephine biopsy
Authors: Diebold J , Molina T , Camilleri‐Broët S , Le Tourneau A , Audouin J 
Published: March 2003

Bone marrow modifications resulting from infections and systemic diseases can be studied by analysis of morphology and aetiology. Two types of lesions or modifications can be observed, those occurring in the connective tissue comprising inflammatory processes, acute and chronic, as well as immune reactions, and those involving the normal haematopoietic cell lines, with possible hyperplastic or aplastic changes in one or more cell lines. The main lesions are described (oedema, haemorrhage, necrosis, suppuration, granulomas, lymphoid nodules and hyperplasia, immunoblastic or plasmacytic hyperplasia), as well as the main aetiologies. In association, the three main haematopoietic cell lines show hyperplasia, hypoplasia, aplasia of one or all of the cell lines, sometimes with dysmyelopoiesis. The stroma and vessel reactions comprise myelofibrosis, gelatinous transformation or amyloid deposits.The methods for identifying aetiological agents are emphasized. It should also be stressed that malignant neoplasias of different types involving the bone marrow can be responsible for such inflammatory or immune reactions.
Expression of CD34 and bcl‐2 in phyllodes tumours, fibroadenomas and spindle cell lesions of the breast
Authors: Moore T , Lee A H S 
Published: March 2003

Strong expression of CD34 and bcl‐2 has been described in solitary fibrous tumours. It has been proposed that these lesions arise from long‐lived mesenchymal cells. We tested the hypothesis that spindle cell lesions of the breast arise from similar mesenchymal cells in the mammary stroma.Sections of phyllodes tumours (26), fibroadenomas (15), myofibroblastomas (two), pseudoangiomatous hyperplasia (five) and myoid hamartoma (one) were stained immunohistochemically for CD34 and bcl‐2. Conventional mammary carcinoma is known to be CD34‐negative: we therefore stained 11 spindle cell carcinomas and one adenosquamous carcinoma. The mammary stroma, particularly around lobules, stained for CD34. All the lesions (except the carcinomas) showed spindle cell staining for CD34. There was more staining in fibroadenomas than in phyllodes tumours (especially malignant tumours). The staining in phyllodes tumours was typically patchy. In some there was increased or decreased staining adjacent to the epithelium. There were occasional spindle cells positive for bcl‐2 in the normal perilobular stroma. bcl‐2 was frequently expressed in spindle cells in fibroadenomas, phyllodes tumours and pseudoangiomatous hyperplasia, and rarely in the other lesions.The combined expression of CD34 and bcl‐2 suggests that fibroadenomas, phyllodes tumours and pseudoangiomatous hyperplasia may arise from long‐lived bcl‐2‐positive mesenchymal cells in the breast in a manner similar to that proposed for solitary fibrous tumours. The absence of CD34 staining in spindle cell carcinomas is of potential diagnostic value in the distinction from malignant phyllodes tumours in difficult cases.
Inflammatory pseudotumour (inflammatory myofibroblastic tumour) of the pancreas: a report of six cases associated with obliterative phlebitis
Authors: Wreesmann V , Van Eijck C H J , Naus D C W H , Van Velthuysen M‐L F , Jeekel J , Mooi W J 
Published: March 2003

Aims:To describe in detail an uncommon pancreatic condition, which generally presents with cholestasis and a mass lesion suspicious of malignancy, and which is characterized histologically by proliferation of fibrous tissue with associated moderate or marked inflammation, as well as obliterative phlebitis.Methods and results:Out of a consecutive series of 23 pancreaticoduodenectomy specimens which on histological evaluation were found to contain no malignant tumour, six cases characterized by the features mentioned above were identified and investigated further. Poor circumscription, firm consistence, histology of dense sclerosis with scattered round cell infiltrates and associated obliterative phlebitis and often perineural accentuation of inflammation were the distinguishing features. On the basis of available histoloigical evidence, the term inflammatory pseudotumour perhaps remains the term best suited to designate this entity, since it sums up its two most distinctive features. However, the possibility that this lesion is in fact a neoplastic process with reactive inflammation (inflammatory myofibroblastic tumour) cannot be ruled out on the basis of the histology, and remains a serious consideration in view of the proven neoplastic nature of lesions with very similar histology arising elsewhere in the body. Importantly, none of the pancreatic lesions reported here recurred or progressed (five informative cases, median follow‐up time 70 months).Conclusions:Inflammatory pseudotumour (inflammatory myofibroblastic tumour) of the pancreas may closely mimic pancreatic adenocarcinoma clinically and radiologically.
Evidence that neurones accumulating amyloid can undergo lysis to form amyloid plaques in Alzheimer's disease
Authors: D'Andrea M R , Nagele R G , Wang H‐Y , Peterson P A , Lee D H S 
Published: March 2003

Aims:Amyloid has recently been shown to accumulate intracellularly in the brains of patients with Alzheimer's disease (AD), yet amyloid plaques are generally thought to arise from gradual extracellular amyloid deposition. We have investigated the possibility of a link between these two apparently conflicting observations.Methods and results:Immunohistochemistry and digital image analysis was used to examine the detailed localization of β‐amyloid42 (Aβ42), a major component of amyloid plaques, in the entorhinal cortex and hippocampus of AD brains. Aβ42 first selectively accumulates in the perikaryon of pyramidal cells as discrete, granules that appear to be cathepsin D‐positive, suggesting that they may represent lysosomes or lysosome‐derived structures. AD brain regions abundantly populated with pyramidal neurones exhibiting excessive Aβ42 accumulations also contained evidence of neuronal lysis. Lysis of these Aβ42‐burdened neurones apparently resulted in a local, radial dispersion of their cytoplasmic contents, including Aβ42 and lysosomal enzymes, into the surrounding extracellular space. A nuclear remnant was found at the dense core of many amyloid plaques, strengthening the idea that each amyloid plaque represents the end product of a single neuronal cell lysis. The inverse relationship between the amyloid plaque density and pyramidal cell density in the AD brain regions also supports this possibility, as does the close correlation between plaque size and the size of local pyramidal cells.Conclusions:Our findings suggest that excessive intracellular accumulation of Aβ42‐positive material in pyramidal cells can result in cell lysis, and that cell lysis is an important source of amyloid plaques and neuronal loss in AD brains.
Use of a monoclonal antibody against Lafora bodies for the immunocytochemical study of ground‐glass inclusions in hepatocytes due to cyanamide
Authors: Hashimoto K , Hoshii Y , Takahashi M , Mitsuno S , Hanai N , Watanabe Y , Ishihara T 
Published: March 2003

Use of a monoclonal antibody against Lafora bodies for the immunocytochemical study of ground‐glass inclusions in hepatocytes due to cyanamide Aims: Ground‐glass inclusions (GGIs) in hepatocytes are known to be associated with cyanamide treatment in patients with alcohol dependency. The purpose of this study was to assess the reactivity of a monoclonal antibody (MAb) raised against polyglucosan and to detect early events in GGI formation. Methods and results: Formalin‐fixed paraffin‐embedded liver tissues from four patients treated with cyanamide were used. Sections were stained with haematoxylin and eosin and periodic acid–Schiff with and without diastase digestion, and were immunohistochemically stained with the MAb. For electron microscopic study, routinely processed liver tissue from one patient was examined with conventional and immunoelectron microscopy with use of the MAb. All specimens from the four cyanamide‐treated patients contained GGIs in the cytoplasm of hepatocytes, and these GGIs reacted intensely with the MAb. Fully developed GGIs contained various organelles, whereas early ones consisted primarily of glycogen granules and dilated smooth endoplasmic reticulum. In immunoelectron microscopic preparations, gold particles were located within GGIs, and the immunolabelled organelles appeared to be glycogen granules. Conclusions: This novel MAb is useful for the detection of GGIs caused by cyanamide. Our results support the idea that GGI formation may result from specific abnormalities in glucose metabolism.
Two relatively distinct patterns of ameloblastoma: an anti‐apoptotic proliferating site in the outer layer (periphery) and a pro‐apoptotic differentiating site in the inner layer (centre)
Authors: Sandra F , Nakamura N , Mitsuyasu T , Shiratsuchi Y , Ohishi M 
Published: March 2003

Two relatively distinct patterns of ameloblastoma: an anti‐apoptotic proliferating site in the outer layer (periphery) and a pro‐apoptotic differentiating site in the inner layer (centre) Aims: This study was performed to determine the apoptotic behaviour of ameloblastomas by analysing the role of bcl‐2 family proteins in ameloblastomas and the location of terminally apoptotic cells in the ameloblastoma epithelial tissues. Methods and results: For immunohistochemistry, tissue sections of 32 patients were treated with an antigen‐retrieval method. Primary antibodies against the apoptosis‐related proteins, bcl‐2, bcl‐X, bax, and bak were applied. Besides immunohistochemistry, Western blotting and TUNEL were also performed. Most of the outer layer cells were predominantly stained by the bcl‐2 antibody, while most of the inner layer cells were stained by antibodies against the apoptosis‐modulating proteins, bax and bak. Among the bcl‐2 family, bcl‐2 was the most ubiquitously expressed protein in ameloblastomas, while bcl‐X was expressed in the greatest concentrations. The major bcl‐X protein was bcl‐XL. Some of the inner layer cells entered the terminal apoptotic stage, which were revealed by TUNEL. The acanthomatous areas over‐expressed the apoptosis‐modulating proteins, especially bak. Conclusions: Ameloblastoma has much more apoptosis‐inhibiting protein than the apoptosis‐modulating protein. Ameloblastoma has two relatively distinct patterns, an anti‐apoptotic proliferating site in the outer layer (periphery) and a pro‐apoptotic differentiating site in the inner layer (centre). The acanthomatous area, which was stained strongly by bak antibody and contained numerous terminally apoptotic cells, was considered as the differentiated area.
Immunohistochemical staining for calretinin is useful in the diagnosis of ovarian sex cord–stromal tumours
Authors: McCluggage W G , Maxwell P 
Published: March 2003

Immunohistochemical staining for calretinin is useful in the diagnosis of ovarian sex cord–stromal tumours Aims: Ovarian sex cord–stromal tumours are a heterogeneous group of neoplasms which may be confused morphologically with a wide variety of tumours. Calretinin positivity has previously been demonstrated in a small number of ovarian sex cord–stromal tumours. The aim of this study was to investigate calretinin staining in a series of these tumours and their histological mimics in order to determine the value of calretinin staining in a diagnostic setting. Methods and results: Seventy‐two neoplasms, including 37 ovarian sex cord–stromal tumours and 35 miscellaneous neoplasms which may enter into the differential diagnosis, were stained with a commercially available polyclonal antibody against calretinin. All sex cord–stromal tumours exhibited positivity except for a single fibrothecoma. In this group of tumours staining was generally diffuse and strong. Small numbers of the miscellaneous group of neoplasms exhibited positivity but this tended to be focal and weak, although this was not always the case. There was consistent strong positive staining of granulosa cells in follicular cysts and corpora lutea. There was also positive staining of luteinized stromal cells in two cases of ovarian stromal hyperplasia and hyperthecosis. Conclusions: Calretinin is a sensitive immunohistochemical marker of ovarian sex cord–stromal tumours and may be useful in a diagnostic setting. However, the value is somewhat limited since occasional neoplasms which enter into the morphological differential diagnosis may be positive. Be that as it may, calretinin positivity may be of value in the diagnosis of an ovarian sex cord–stromal tumour and its differentiation from other neoplasms. In this regard, calretinin should always be used as part of a larger panel.