bluuebunny/crossref_metadata_2025_split huggingface dataset:
Translocation (11;14): A cytogenetic anomaly associated with B‐cell lymphomas of non‐follicle centre cell lineage
Authors: Vandenberghe Elisabeth , De Wolf‐Peeters Chris , Van Den Oord Joost , Wlodarska Ivonna , Delabie Jan , Stul Michel , Thomas José , Michaux Jean‐Louis , Mecucci Cristina , Cassiman Jean‐Jacques , Van Den Berghe Herman 
Published: June 2005

AbstractNine patients with t(11;14) and B non‐Hodgkin's lymphomas composed of small to intermediately sized cells with irregular nuclei are described. Immunophenotyping was performed on seven cases, which were M+, D− with light chain restriction, CD5+, CD10−, and CD20+, suggesting that they were non‐follicle centre cell lymphomas. The translocation (11;14) (in three cases the only cytogenetic anomaly) was associated with rearrangement of bcl‐1 in four of the five cases investigated. Translocation (11;14) has been described in an apparently heterogeneous group of low‐grade lymphoid malignancies which we suggest have a non‐follicle centre cell lineage in common. This translocation may be associated with these lymphomas in the same way that t(14; 18) is associated with follicle centre cell lymphomas.
Histopathological grading of soft tissue tumours. Prognostic significance in a prospective study of 278 consecutive cases
Authors: Jensen Olaf Myhre , Høgh Jørgen , Østgaard Svend E. , Nordentoft Axel Munck , Sneppen Otto 
Published: June 2005

AbstractA consecutive 10‐year series of 278 soft tissue sarcomas was prospectively graded, using a system based on the number of mitoses and taking into account parameters such as cellularity, anaplasia, necrosis, and histogenetic type and subtype of tumour. Prognostic factors in relation to metastasis‐free survival were studied by uni‐ and multivariate analysis.Fifty‐seven (20·5 per cent) were low‐grade tumours, 43 (15·5 per cent) were intermediate, and 178 (64 per cent) were high grade. High‐grade tumours were divided into two groups; 80 (29 per cent) grade 3A (=5–20 mitoses per 10 high power fields (HPF)) and 78 grade 3B (28 per cent) (=more than 20 mitoses/10 HPF); 10 HPF corresponds to 2·5 mm2. Twenty (7·2 per cent) high‐grade tumours could not be further subdivided.Grading was found to be the prognostic factor associated with the strongest predictive value. Five‐year survival in low‐grade and intermediate tumours (95 and 86 per cent, respectively) differed significantly (P < 0·0001) from high grade (50 per cent) and (P = 0·0018) between grade 3A (64 per cent) and grade 3B (41 per cent). Other prognostic indicators of importance in high‐grade tumours were age, local recurrence at presentation (primary operation outside the Centre), and localization (superficial vs. deep).
‘Neuroendocrine’ differentiation in primary neoplasms of the liver
Authors: Wang Jiahua , Dhillon Amar P. , Sankey Elizabeth A. , Wightman A. Kay , Lewin Jackie F. , Scheuer Peter J. 
Published: June 2005

AbstractThirty primary liver neoplasms (16 hepatocellular, nine biliary, and five epithelioid haemangioendotheliomas) were studied for the expression of the general ‘neuroendocrine’ markers, neurone specific enolase (NSE) and protein gene product 9·5 (PGP 9·5). Grimelius silver staining for neurosecretory granules and immunostaining for S100 protein, HMB‐45, vasoactive intestinal polypeptide (VIP), and calcitonin were also performed. Eleven of the 16 hepatocellular carcinomas stained positively for PGP 9·5, four for NSE, six for HMB‐45, and two for S100 protein. Seven exhibited granular staining by the Grimelius method; eight showed immunostaining for VIP, and two for calcitonin. Three of the five haemangioendotheliomas demonstrated positive immunostaining for PGP 9·5, and two for NSE; of the nine biliary carcinomas, two showed staining for PGP 9·5 and NSE, and four contained cells staining with the Grimelius technique. Primary neoplasms of liver may show ‘neuroendocrine’ differentiation and this aspect of their phenotypic expression has to be considered before predicting the site of origin of a tumour in the liver.
Binding of ubiquitin to experimentally induced murine AA amyloid
Authors: Chronopoulos Soula , Alizadeh‐Khiavi K. , Normand Josée , Ali‐Khan Z. 
Published: June 2005

AbstractAmyloid enhancing factor (AEF) activity has recently been demonstrated in ubiquitin purified from amyloidotic murine tissues and Alzheimer brain extract. Since AEF is known to bind to amyloid fibrils and ‘fibril‐AEF’ on passive transfer induces accelerated amyloidogenesis in the recipient animals, it was of interest to investigate whether ubiquitin binds to amyloid. Immunohistological studies were carried out on liver sections from amyloidotic mice. Biotin–strepavidin–peroxidase methods using monospecific rabbit anti‐mouse AA amyloid IgG (RAAG) and rabbit anti‐bovine ubiquitin IgG (RABU) antibodies were employed to immunostain the amyloid and ubiquitin deposits, respectively. RABU‐treated liver sections were counterstained with thioflavine S. RAAG reacted strongly with the amyloid, indicating that it is AA type, and RABU‐positive immunodeposits were found bound to the thioflavine‐S‐positive AA deposits. Treatment of the liver sections with 0·1 M sodium acetate containing 0·5 M NaCl, pH 4, for 2–3 h at 37°C nearly completely desorbed the AA amyloid‐bound ubiquitin. Since ubiquitin demonstrates AEF activity in vivo and binds non‐covalently to AA amyloid, we suggest that ubiquitin may indeed be ‘fibril‐AEF’ and may play a crucial role in the pathogenesis of amyloidosis. To our knowledge, this is the first time that ubiquitin bound to extracellularly deposited amyloid has been demonstrated.
Is focal chronic autoimmune thyroiditis an age‐related disease? Differences in incidence and severity between Japanese and British
Authors: Okayasu Isao , Hatakeyama Shigeru , Tanaka Yasukazu , Sakurai Tetsushi , Hoshi Kazuo , Lewis Paul D. 
Published: June 2005

AbstractThe incidence of chronic lymphocytic thyroiditis in autopsy material from Japanese and British subjects was evaluated. Lymphocytic infiltration in representative thyroid sections from 1826 Japanese cases collected from four different institutions was analysed. The overall incidence of lymphocytic infiltration was significantly higher in females (22·2 per cent) than in males (13·9 percent). In females, the incidence reached 23·2 percent in the fourth decade and showed no increase with age thereafter. The overall incidence of lymphocytic infiltration in thyroid sections from 810 British cases was 42·5 per cent in females and 19·4 per cent in males: an increase in the incidence of thyroiditis from the sixth decade onwards was noted in British females, the figure reaching 50·0 per cent in those aged over 70 years. These findings suggest possible racial differences in susceptibility to chronic thyroiditis. The disorder is not necessarily related to age, increasing severity of disease with age being found only in British females.
Distribution of β1, α1, α2 and α3 integrin chains in basal cell carcinomas
Authors: Stamp G. W. H. , Pignatelli M. 
Published: June 2005

AbstractThe integrins are αβ heterodimeric transmembrane proteins mediating cell–substratum as well as cell‐cell interactions. Changes in their expression and/or function seem to occur in a number of malignant epithelial neoplasms and may in part explain their abnormal patterns of growth and differentiation. Using monoclonal antibodies to the β1 (DH12), α1 (TS2/7), α2 (B1.515), and α3 (E1.56) integrin chains, the α1β1 (VLA‐1), α2β1 (VLA‐2), and α3β1 (VLA‐3) integrin receptors were studied on cryostat sections of 22 basal cell carcinomas (BCCs) and adjacent normal tissues by a standard peroxidase‐antiperoxidase technique. In non‐neoplastic skin, VLA‐2 and VLA‐3 were found in the basal layer, eccrine glands, and cells of the outer root sheath in which VLA‐1 was detected. In BCCs, there was a considerably higher expression of VLA‐2 and VLA‐3 compared with epidermal basal cells but similar to that seen in hair bulb and outer root sheath. In two cases of nodular BCC showing evidence of regression, both VLA‐2 and VLA‐3 were completely negative, in contrast to non‐regressing foci which were strongly positive.The high level of expression of two adhesion molecules (VLA‐2 and VLA‐3) involved in cell‐substratum as well as cell‐cell interactions may account for the more indolent pattern of growth characteristic of BCC and perhaps reflect its high degree of differentiation towards the hair follicle.
A new monoclonal antibody, PM‐2K, specifically recognizes tissue macrophages but not blood monocytes
Authors: Takeya Motohiro , Tsuchiya Tatsuaki , Shimokawa Yasuhiro , Takahashi Kiyoshi 
Published: June 2005

AbstractA new monoclonal antibody, PM‐2K, was raised against 24‐h cultured human peritoneal macrophages. Immunohistochemically, PM‐2K recognized most tissue macrophages in lymphoreticular organs such as the thymus, spleen, lymph node, and tonsil. Kupffer cells of the liver, alveolar macrophages, and macrophages in the interstitial tissue of the kidney, pancreas, and many other organs were also positively labelled. On the other hand, PM‐2K failed to recognize blood monocytes, freshly isolated peritoneal macrophages, microglial cells, osteoclasts, and dendritic cells such as Langerhans cells, interdigitating cells, and follicular dendritic cells. In various pathological conditions. PM‐2K labelled a wide variety of proliferating macrophages. Reaction products of PM‐2K were observed by immunoelectron microscopy on the cytoplasmic membrane of cultured peritoneal macrophages. The molecular weight of the antigen recognized by PM‐2K was determined to be 150 kD by Western blotting. As no cells other than macrophages were reactive with PM‐2K, this antibody is considered to be very useful not only in the investigation of macrophage differentiation and maturation, but also in the diagnosis of various proliferative disorders of macrophages.
p53 expression in human breast cancer related to survival and prognostic factors: An immunohistochemical study
Authors: Ostrowski J. L. , Sawan A. , Henry L. , Wright C. , Henry J. A. , Hennessy C. , Lennard T. J. W. , Angus B. , Horne C. H. W. 
Published: June 2005

AbstractIn a study of 90 breast cancer patients, tumour p53 protein expression was determined by immunohistochemistry using the monoclonal antibody PAb1801. Patient lymph node status and Bloom's grade were determined, and both oestrogen and progesterone status assessed, also by immunohistochemistry. Lymph node status, tumour grade, and progesterone receptor status all had a significant influence on survival. Patients with p53‐positive tumours showed poorer survival but this did not achieve significance. p53 protein expression showed a significant relationship to high tumour grade and a weak correlation with negative oestrogen receptor status. The data suggest taht p53 protein expression may be a marker of more aggressive carcinomas but that the prognostic power of expression is likely to be weak and unlikely, therefore, to be of clinical value. The results do not resolve whether detectable p53 protein expression represents a random product of dedifferentiation, or an important feature of the malignant phenotype, playing a key role in tumour behaviour. The number of patients in our study is small, however, and investigation of a larger series is clearly indicated.
Histopathological studies on the local reactions induced by complete fReund's adjuvant (CFA), bacterial lipopolysaccharide (LPS), and synthetic lipopeptide (P3C) conjugates
Authors: Wiedemann Frank , Link Ralf , Pumpe Konrad , Jacobshagen Ulrich , Schaefer Hans E. , Wiesmüller Karl‐Heinz , Hummel Rolf‐Peter , Jung Günther , Bessler Wolfgang , Böltz Traudel 
Published: June 2005

AbstractThe inflammatory reactions following subcutaneous application of adjuvants revealed characteristic pathological patterns. The injection of complete Freund's adjuvant (CFA) resulted in the formation of large lipid deposits encircled by an inflammatory reaction and concentrically arranged collagen bundles. Bacterial lipopolysaccharide (LPS) caused granulomatous aggregations of mononuclear cells with thrombotic vessel occlusions. Inoculation of the lipopeptide adjuvants induced accumulation of mononculear cells with only minimal fibrotic changes which were resolved after day 28. Lipopeptide conjugates based on the head group tripalmitoyl‐S‐glyceryl‐cysteinyl‐serin (P3CS) can thus be used as effective immunogens and adjuvants without long‐term tissue damage.
Phenotypic modulation in lipocytes in experimental liver fibrosis
Authors: Tanaka Yujiro , Nouchi Toshihiko , Yamane Michio , Irie Tetsuya , Miyakawa Happei , Sato Chifumi , Marumo Fumiaki 
Published: June 2005

AbstractThe presence of a‐smooth muscle actin (smA)‐positive cells has recently been reported in the fibrotic liver. Lipocytes have been considered to play important roles in hepatic fibrosis. However, the relation of the a‐smA‐positive cells and lipocytes has not been determined. The biological implication of a‐smA expression remains unknown. To study these questions, we carried out double immunofluorescent staining of a‐smA and desmin (a marker for lipocytes), or a‐smA and collagen, and double immunohistochemical staining of a‐smA and 5‐bromo‐2′‐deoxyuridine (BrdUrd) in carbon tetrachloride‐induced fibrotic rat livers. In normal and control livers, a‐smA‐positive cells were not seen in the lobules, whereas scattered desmin‐positive cells were present. With the development of hepatic fibrosis, a‐smA was expressed only in a portion of desmin‐positive cells located predominantly around collagen bundles. A number of a‐smA‐positive cells in the lobules were labelled with BrdUrd. These results suggest phenotypic modulation in lipocytes and differentiation of lipocytes towards myofibroblast‐like cells, since a‐smA is expressed with desmin in myofibroblasts in scar tissue. The expression of a‐smA may be related to events of the fibrotic process, such as tissue contraction or fibrogenesis per se.
Low expression of β1, α2 and α3 subunits of VLA integrins in malignant mammary tumours
Authors: Pignatelli Massimo , Hanby Andrew M. , Stamp Gordon W. H. 
Published: June 2005

AbstractThe Very Late Antigens (VLAs) are αβ heterodimeric transmembrane proteins mediating cell–substratum as well as cell–cell interactions. Changes in their expression and/or function seem to occur in a number of invasive carcinomas and may at least in part explain their abnormal patterns of growth and differentiation. Using monoclonal antibodies to the β1 (DH12, A1A‐5), α2 (B1.515) and α3 (E1.56) chains, VLA‐2 (α2β1) and VLA‐3 (α3β1) were studied on cryostat sections of three fibroadenomas and 43 invasive breast carcinomas (29 ductal, 14 lobular) by the avidin–biotin complex immunoperioxidase technique. In non‐neoplastic breast tissue and in fibroadenomas VLA‐2 and VLA‐3 were expressed by myoepithelial cells and on the basolateral surface of the luminal cells. There was weak or absent expression of α2, α3 and the common β1 chain in the majority of invasive carcinomas compared to the adjacent normal breast epithelium and preinvasive (in‐situ) carcinomas. In addition, the expression of the α2 chain of VLA‐2 was reduced significantly (P < 0.005) in the poorly differentiated ductal breast carcinomas (Grade III) compared to the well (Grade I) and moderately (Grade II) differentiated ductal tumours. These data give further evidence that loss or down‐regulation of VLA‐2 and VLA‐3 occur relatively frequently in invasive cancers, and, at least in the invasive ductal breast carcinomas. Loss of an extracellular matrix receptor controlling growth and differentiation seems to be one of the abnormalities underlying the progression towards an undifferentiated morphology.
Unilateral papillary necrosis complicating renal artery stenosis—evidence of activation of the intrarenal renin–angiotensin system?
Authors: Lindop George B. M. , Raweily Essam A. , Graham Patricia C. 
Published: June 2005

AbstractWe report an association between renal artery stenosis and papillary necrosis. We studied three kidneys with renal artery stenosis, two of which showed ipsilateral acute papillary necrosis. In all three cases there had been a sudden fall in perfusion of the ischaemic kidney. In the case with intact papillac, immunostainable renin was normal in amount and distribution, whereas both kidneys with papillary necrosis showed hyperplasia of renin‐containing cells, and these were mainly in the JGAs of the juxtamedullary cortex. Since the contralateral kidneys were spared, we suggest that in an ischaemic kidney with hyperplasia of renin‐secreting cells in the deep cortex, local activation of the renin‐angiotensin system could cause acute papillary necrosis due to vasoconstriction.
A comparison of immunohistochemical markers of cell proliferation with experimentally determined growth fraction
Authors: Scott R. J. , Hall P. A. , Haldane J. S. , Van Noorden S. , Price Y. , Lane D. P. , Wright N. A. 
Published: June 2005

AbstractThe relationship between immunoreactivity for cell proliferation markers (Ki67 and PCNA) and the growth fraction as determined by the fraction of labelled mitoses method was assessed in xenograft tumours grown from the LoVo cell line in nude mice. FLM curves were constructed by injecting tritiated thymidine and then preparing autoradiographs from the tumours. From this data an estimate of growth fraction and cell cycle time were made. Using frozen material from the same tumours, the Ki67 index was determined by immunostaining. PCNA staining was determined in the fixed material which had been used for the autoradiographs. The results show that Ki67 staining follows the same trend as the FLM‐determined growth fraction as the tumour increases in size and the rate of growth decreases. However the Ki67 index does produce a consistent overstimate of the growth fraction in this in‐vivo system, as compared to observations in cell culture. PCNA staining showed virtually 100 per cent positive staining in all the tumours, which is likely to reflect the long half‐life of the antigen, compared to the very fast cell‐cycle time of the xenograft tumours. These results show that staining with proliferation markers is not a precise determinant of growth fraction. Ki67 staining is a method that can be usefully applied as an operational marker of cell proliferation, but should not be used uncritically. Further caution is necessary in the use of PCNA. The findings also demonstrate the need to use a range of methods when assessing a new proliferation marker.
Morphometric analysis of Mycobacterium tuberculosis infection in mice suggests a genetic influence on the generation of the granulomatous inflammatory response
Authors: Orrell J. M. , Brett S. J. , Ivanyi J. , Coghill G. , Grant A. , Beck J. Swanson 
Published: June 2005

AbstractThere is evidence in natural human disease and experimental infection in mice that host genetic factors influence susceptibility to infection with Mycobacterium tuberculosis and the progress of the disease. In mouse models, both H‐2 and non‐H‐2 genes have been implicated. In this study, four inbred strains of mice (Balb/b, Balb/k, B10, B10.BR), selected for combinations of two different H‐2 haplotypes on two different non‐H‐2 backgrounds, were inoculated with M. tuberculosis, strain H37Rv, by intraperitoneal injection. The histological features of the granulomatous inflammatory response in the liver and lungs were investigated during the first 18 weeks of the infection. Granuloma fraction, mean granuloma area, bacillary load, and the density of acid‐fast bacilli within granulomata were measured. Animals of all four strains showed the same general pattern of infection with an early, and later self‐limiting, infection of the liver and delayed onset, but progressive, infection of the lung. The non‐H‐2 related genetic background appears to influence the morphology of the granulomatous inflammatory response. In comparison, H‐2 differences appeared to be small and inconsistent.
Rapid acinar to ductal transdifferentiation in cultured human exocrine pancreas
Authors: Hall P. A. , Lemoine N. R. 
Published: June 2005

AbstractExperiments have been performed to define conditions for the primary culture of human exocrine pancreas, as a first step towards molecular reconstruction experiments of pancreatic neoplasia. Normal human exocrine pancreas was digested using collagenase and dispase and the resulting cellular aggregates were cultured in vitro. The phenotype of the digested pancreatic cells was almost exclusively acinar (amylase‐positive, keratin 19 and mucin antigens‐negative), Yet within 4 days of culture the cells had taken on a ductal phenotype (amylase‐negative, keratin 19 and mucin antigens positive). The kinetics of these observations exclude the possibility of overgrowth of the acinar population by a ductal sub‐population, and selective adherence is excluded by examination of those cells that do not adhere, which are representative of the initiating population. We interpret these data as indicating that, under the conditions of culture, the acinar cell phenotype is not stable and can transdifferentiate to a ductal phenotype. Taken together with recent data from transgenic animals, this in vitro observation has possible implications for our view of the pathogenesis of pancreatic neoplasia.
T‐Cell receptor variable (V) gene usage by lymphoid populations in T‐cell lymphoma
Authors: Smith John L. , Lane Andrew C. , Hodges Elizabeth , Reynolds Wendy M. , Howell William M. , Jones David B. , Janson Carl H. 
Published: June 2005

AbstractA panel of monoclonal antibodies specific for TcR V gene families was used to study TcR V region expression in 28 cases of malignant and reactive T‐cell expansions including four cases of mixed cellularity Hodgkin's disease (HD) and five reactive cases. TcR Vβ5 gene products were represented in three cases of lymphoblastic malignancy (Vβ5.1, Vβ5.2) and two cases of peripheral T‐cell lymphoma (PTCL) (Vβ5.1). In the PTCL cases, the expanded family was found in the absence of clonal TcR gene rearrangements and in one of these cases with Ig JH and Ck clonal gene rearrangements consistent with the presence of a phenotypically and histologically undetectable clonal B‐cell population. In a third PTCL case not investigated for genotype, the TCR Va12 family was overrepresented. Expanded TcR Va2 and Vβ5.1 families were identified in HD and Vβ8 and Vβ5.2/Vβ5.3 families in a reactive lymph node and CD3 and CD8‐positive blood lymphocytosis respectively. Further study of PTCL and related entities are needed to establish whether expanded TcR families are common in those cases that fail to exhibit clonal TcR gene rearrangement.