bluuebunny/crossref_metadata_2025_split huggingface dataset:
The expression of the trefoil peptides pS2 and human spasmolytic polypeptide (hSP) in ‘gastric metaplasia’ of the proximal duodenum: Implications for the nature of ‘gastric metaplasia’
Authors: Hanby Andrew M. , Poulsom Richard , Elia George , Singh Sukhdev , Longcroft Janet M. , Wright Nicholas A. 
Published: June 2005

AbstractExpression of pS2 protein (an oestrogen‐induced gene discovered in the MCF‐7 breast carcinoma cell line) and its homologue human spasmolytic polypeptide (hSP) was analysed, using immunohistochemistry and in situ hybridization to their mRNAs, in the proximal duodenum of 17 partial gastrectomy specimens removed from individuals with chronic peptic ulceration. Eight were found to have gastric‐type metaplasia. In gastric metaplasia, mRNAs for pS2 and hSP, and pS2 peptide antibody were co‐localized in the cells covering the duodenal villi, pS2 immunostaining was diffusely cytoplasmic in nature. A similar pattern was seen in Brunner's gland ducts. The trefoil peptide localization in gastric metaplasia closely resembles that seen in superficial gastric epithelium and the distal Brunner's gland duct, which in turn shares morphological similarities with gastric epithelium. We therefore conclude that gastric metaplasia may be the result of an expansion of the surface component of the Brunner's gland duct. The function of these trefoil peptides is at present unknown, but their distribution elsewhere suggests an involvement in reparative mechanisms. The similarities between gastric foveolar and Brunner's gland duct epithelium may derive from common restitution‐enhancing features pertinent to a locally harsh environment.
Cartilage and bone formation in repairing achilles tendons within diffusion chambers: Evidence for tendon–cartilage and cartilage–bone conversionin vivo
Authors: Rooney Paul , Walker Duncan , Grant Michael E. , McClure John 
Published: June 2005

AbstractRodent Achilles tendons were subjected to midpoint tenotomy and allowed to recover for various times in situ before the operated tissue was removed, placed into a Millipore diffusion chamber, and inserted intraperitoneally into syngeneic hosts. Diffusion chambers were then removed at weekly intervals, such that the total time after the operation (i.e., time allowed to recover in situ plus time within the diffusion chamber) was up to 8 weeks, and examined histologically. Ectopic cartilage was produced within the diffusion chamber after a total of 4 weeks but only if the first 2 weeks of recovery were in situ. With increasing time, calcified cartilage, osteoid and bone were also observed. Overall, the evidence suggests that the cartilage forms via a direct conversion from tendon tissue and that the bone may form as a result of differentiative changes of hypertrophic chondrocytes.
Comparison between the monoclonal antibodies Ki‐67 and PC 10 in 125 malignant lymphomas
Authors: Sabattini Elena , Gerdes Johannes , Gherlinzoni Filippo , Poggi Simonetta , Zucchini Luca , Origioni Giuseppe Meliell Francesco , Del Vecchio Maria T. , Leoncini Lorenzo , Falini Brunangelo , Pileri Stefano A. 
Published: June 2005

AbstractThe monoclonal antibody (MAb) Ki‐67 detects a nuclear proliferation‐associated antigen which corresponds to a non‐histone protein with a molecular weight of 395 and 345 kD. Its prognostic relevance has been assessed in both lymphoid and non‐lymphoid tumours. The MAb PC10 picks up the proliferating cell nuclear antigen (PCNA), which is a 36 kD nuclear protein associated with the cell cycle Whereas Ki‐67 works only in fresh material. PC10 detects a fixation‐resistant epitope of PCNA. Preliminary data have revealed a linear relationship between Ki‐67 and PC 10 reactivity in normal lymphoid tissue and in non‐Hodgkin's lymphomas (NHLs). We applied Ki‐67 and PC 10 to frozen and routine sections, respectively, from 25 examples of Hodgkin's disease (HD) (14 nodular sclerosis, 6 lymphocyte predominance, 5 mixed cellularity) and 100 NHLs (corresponding to the main varieties of the updated Kiel classification). The results obtained can be summarized as follows: (1) both MAbs gave rise to extremely variable results within the same category of NHLs; (2) most Hodgkin and Reed‐Stern berg cells (50‐98 per cent) were labelled by the reagents; (3) Ki‐67 and PC10 stained a similar ratio of neoplastic cells in 65 and 76 per cent of NHL and HD cases, respectively; in the remaining instances, no correspondence was observed, the PC10‐positive elements usually outnumbering the Ki‐67‐positive ones significantly. These discrepancies, which might be due to low PCNA catabolism and/or PCNA expression by quiescent cells, underline the need for further kinetic and clinico‐pathologic studies in order to define the specific relevance of PC 10.
Molecular mechanisms involved in intraepithelial lymphocyte migration: A comparative study in skin and tonsil
Authors: Uccini Stefania , Ruco Luigi P. , Monardo Francesca , La Parola Ilaria Lesnoni , Cerimele Decio , Baroni Carlo D. 
Published: June 2005

AbstractIntraepithelial lymphocyte migration is a biological process frequently observed in skin and tonsil. Using immuno‐histochemistry, we have studied the molecular bases of this process in seven skin biopsies involved by mycosis fungoides (MF) and in 12 tonsils, four involved by B‐chronic lymphocytic leukaemia (B‐CLL) and eight by lymphoid follicular hyperplasia (LH). In the skin, intraepidermal T‐lymphocyte infiltration was associated with narrowing and fragmentation of the basement membrane, as shown by an anti‐collagen type IV antibody. Immunostaining of serial sections with an anti‐collagenase type IV antibody revealed that collagenase type IV was localized in the upper dermis and Strictly co‐distributed with collagen type IV, suggesting that enzymatic digestion played a role in the alterations of the basement membrane. Further migration through the epidermis was mediated by expression on keratinocytes of intercellular adhesion molecule‐1 (ICAM‐1) and of leukocyte‐function associated antigen‐1 (LFA‐1) on infiltrating lymphocytes. In the tonsil, intraepithelial infiltration was mediated by the expression of vascular cell adhesion molecule‐1 (VCAM‐1) by epithelial cells and of very late antigen‐4 (VLA‐4) by infiltrating lymphocytes. Further intraepithelial lymphocyte migration was then established, as already shown in the skin, by ICAM‐1/LFA‐1 interaction. Lymphocyte recruitment from the systemic circulation was studied using antibodies directed against endothelial leukocyte adhesion molecule‐1 (ELAM‐1), ICAM‐1, and VCAM‐1. These adhesion molecules were highly expressed by blood vessels in the upper dermis of MF and the percentage of ELAM‐1 +/VCAM‐1 + vessels was significantly higher than that observed in tonsils. Our data suggest that distinct molecular mechanisms are used by lymphocytes in intraepithelial migration in the skin and in tonsils.
Immunohistochemical staining of ras oncogene product in neoplastic and non‐neoplastic mesothelial tissues: Immunoreactivity for N‐ras and lack of immunohistochemical staining for Ha‐ras and K‐ras
Authors: Ramael Marc , Deblier Ivo , Eerdekens Christa , Lemmens Greet , Jacobs Werner , Van Marck Eric 
Published: June 2005

AbstractImmunohistochemical staining of 36 malignant mesothcliomas and 45 cases of non‐neoplastsic mesothelium including 20 specimens with signs of hyperplasia were investigated using murine monoclonal antibodies directed against p21 ras protein, Ha‐ras protein, K‐ras protein, and N‐ras protein. All cases of non‐neoplastic mesothelium and the majority of the malignant mesotheliomas (78 per cent) showed cytoplasmic and often submembranous immunoreactivity in more than 50 per cent of the cells with both the pan‐ras and N‐ras antibody. No immunoreactivity was observed for Ha‐ and K‐ras. There was no statistically significant difference with respect to immunoreactivity between neoplastic and non‐neoplastic mesothelium or between the various mesothelioma subtypes.
Metabolic requirements for phorbol ester‐induced cytoskeletal changes in renal epithelium
Authors: Rahilly Mave A. , Fleming Stewart 
Published: June 2005

AbstractAlteration of the cytoskeleton and cell–substratum adhesion are important in the progression of renal carcinoma. We have previously shown that treatment of normal human renal epithelium with phorbol esters mimics the changes seen in renal carcinoma cells. In this study we have demonstrated that the phorbol ester‐induced cytoskeletal reorganization is inhibited in the presence of deoxyglucose but not by cycloheximide. We have also shown that treatment of cells with cytochalasin B results in the formation of immature stress fibres restricted to the cell–substratum contact regions. These results suggest that the actin filaments elongate from the focal contacts and that structural rearrangement caused by phorbol esters is an energy‐dependent phenomenon but is independent of de novo protein synthesis.
Induction of drug‐metabolizing enzymes in human pancreatic cancer and chronic pancreatitis
Authors: Foster John R. , Idle Jeffrey R. , Hardwick James P. , Bars Remi , Scott Patrick , Braganza Joan M. 
Published: June 2005

AbstractChronic pancreatitis and pancreatic cancer have both been linked with occupational exposure to organic chemicals. These chemicals are known to be metabolized within the liver by the cytochrome P‐450 family of enzymes, and indeed are able to induce levels of these enzymes as evidence of their interaction. The purpose of this study was therefore to see if these enzyme systems were altered in chronic pancreatitis and pancreatic cancer. Immunocytochemistry of four phase I drug‐metabolizing enzymes (cytoxhromes P‐450 IIIA1, P‐450IIE, P‐450 IA2, and NADPH cytochrome P‐450 oxido‐reductase) and one phase II enzyme [glutathione S‐transferase (GST) 5‐5] was therefore performed on pancreas and/or liver biopsy samples from organ donors and compared with patients with chronic pancreatitis or pancreatic cancer. In samples from donor subjects, the types and levels of drug‐metabolizing enzymes in hepatocytes were similar to those seen in pancreatic acinar cells. In material from patients with chronic pancreatitis or pancreatic cancer, cytochrome P‐450 enzyme levels were greater in both the liver and the pancreas than those seen in the donor group, while GST levels were unchanged. Islets of Langerhans showed high levels of P‐450 IA2 in the donor group, with clear induction of P‐450 IIIA1 and NADPH cytochrome P‐450 oxidoreductase in patients with chronic pancreatitis but not in the pancreatic cancer group. Levels of GST 5‐5 were also induced in the islets. The present findings raise the possibility of an aetiological relationship between elevated levels of drug‐metabolizing enzymes and the subsequent development of disease.
Ultimobranchial body nests in human fetal thyroid: An autopsy, histological, and immunohistochemical study in relation to solid cell nests and mucoepidermoid carcinoma of the thyroid
Authors: Harach H. R. , Vujanić G. M. , Jasani B. 
Published: June 2005

AbstractThe mid portion of the lateral thyroid lobes from 64 fetuses was systematically analysed for the presence of ultimobranchial body nests. The nests showed a prevalence of 1 /24 (4.2 per cent) or 13/40 (32.5 per cent) depending on whether a single‐ or a multi‐step sectioning method was employed, respectively, and showed anatomical, morphological, and histochemical features similar to those of ultimobranchial postnatal thyroid solid cell nests. Histochemical studies revealed the presence of mucosubstances in 73 per cent of the cases, calcitonin‐immunoreactive cells in 36 per cent, and both carcinoembryonic antigen and high‐molecular‐weight cytokeratin‐immunoreactive epidermoid cells in 85.7 per cent, respectively. These findings indicate that these markers, which are also expressed by solid cell nests of the thyroid, are of value for the detection and tracing of ultimobranchial tissue to earlier stages of development. The findings of this study support the hypothesis that mucoepidermoid carcinomas of the thyroid are of ultimobranchial tissue origin.
In situ end‐labelling detects DNA strand breaks in apoptosis and other physiological and pathological states
Authors: Ansari B. , Coates P. J. , Greenstein B. D. , Hall P. A. 
Published: June 2005

AbstractWe have investigated the use of a novel technique, in situ end‐labelling, as a means of the specific identification of apoptotic cells in formalin‐fixed, paraffin‐processed tissue sections. The technique relies on the presence of DNA strand breaks in apoptotic cells, caused by activation of endogenous nuclease activity during the process of cell death. These strands are labelled with a non‐isotopic reporter molecule in the presence of a DNA polymerase, and labelled DNA is identified immunohistochemically. We show that in situ end‐labelling stains cells with the morphological characteristics of apoptosis, and greatly simplifies their identification. Furthermore, in two model systems, the number of labelled cells parallels the number of cells undergoing apoptosis as measured by alternative techniques. The ability of the Klenow fragment of DNA polymerase to label apoptotic nuclei suggests that the characteristic DNA fragmentation seen during this process involves the formation of DNA breaks with a 5′ overhang. in situ end‐labelling will be valuable for the identification and quantitation of apoptosis in a range of normal tissues and in a variety of pathological states. However, the technique is not specific for programmed cell death, and results must be interpreted with caution and correlated with morphological criteria of apoptosis.
Sequencing and quantitative assessment of mutant and wild‐type mitochondrial DNA in paraffin sections from cases of MELAS
Authors: Love S. , Nicoll J. A. R. , Kinrade E. 
Published: June 2005

AbstractMELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke‐like episodes) is a clinically devastating disease of children and young adults. The cause of the stroke‐like episodes is not known. We have sequenced the mitochondrial DNA (mtDNA) in archival paraffin‐embedded material from two cases. In only one of these did the mitochondrial tRNALeu(UUR) gene contain the nucleotide 3243 A‐to‐G mutation that is most commonly responsible for MELAS. In this case, we determined the relative proportion of mutant:wild‐type mtDNA in sections of the central nervous system and other tissues by PCR amplification, PalI digestion, DNA electrophoresis, and scanning densitometry of the ethidium bromide‐stained gels. The technique allowed the proportion of mitochondria that contain the mutant genome to be compared with the histological findings in immediately adjacent sections of tissue. The mutant mtDNA was detectable in most tissues, the percentage of mtDNA ranging from barely detectable levels to 78 percent. The relative amount of mutant mtDNA correlated poorly with the distribution of histological lesions, both within the central nervous system and in other tissues examined. The proportion was high in tissues such as liver, kidney, adrenal, and pancreas that appeared histologically normal. Relatively low levels were present in some regions of the central nervous system, such as the occipital lobe, which contained many of the characteristic infarct‐like lesions. These observations do not support previous speculation that the distribution of these lesions reflects that of the defective mitochondria. The results emphasize the usefulness of the polymerase chain reaction in correlative histogenetic studies.
An immunohistochemical study of the long‐term effects of androgen administration on female‐to‐male transsexual breast: A comparison with normal female breast and male breast showing gynaecomastia
Authors: Burgess Helen E. , Shousha Sami 
Published: June 2005

AbstractThis study was aimed at assessing the effects of therapeutic long‐term administration of androgens on normal human female breast. Sections from mastectomy specimens of 29 female‐to‐male transsexuals who had prolonged androgen administration prior to surgery were examined using routine light microscopy and immunohistochemical techniques. For comparison, sections from ten ‘normal’ female breast reduction mammoplasty specimens and ten cases of gynaeco‐mastia were similarly examined. Haematoxylin and eosin‐stained sections were assessed for the prevalence of elements of the normal breast and benign breast lesions. Immunoperoxidase techniques were performed to study the distribution of a variety of breast‐associated antigens and receptors. The results were assessed semi‐quantitatively.The prevalence of normal acini and ducts, fibrosis, cysts, and apocrine metaplasia in transsexual specimens was not statistically different from that seen in normal controls. However, transsexual specimens had a significantly higher prevalence of microcalcification than normals. The majority of transsexual specimens were positive for gross cystic disease fluid protein‐15, lactoferrin, and progesterone and oestrogen receptors, and negative for B72.3 and pS2. These findings were not significantly different from those in normal controls.All ten gynaecomastia specimens were positive for oestrogen and progesterone receptors. The prevalence of oestrogen receptors was significantly higher than that seen in transsexuals and normal controls, but the prevalence of progesterone receptors was only significantly higher than that seen in transsexuals.It is concluded that long‐term androgen administration does not appear to have any significant lasting effect on the normal human female breast, as demonstrated by a wide range of histological and immunohistological criteria.
Increased expression of cytokeratins 8, 18 and vimentin in the invasion front of mucosal squamous cell carcinoma
Authors: Schaafsma H. E. , Velden L.‐A. Van Der , Manni J. J. , Peters H. , Link M. , Ruiter D. J. , Ramaekers F. C. S. 
Published: June 2005

AbstractThe immunohistochemical expression patterns of cytokeratins 8 and 18 and vimentin were examined in frozen sections of 120 human mucosal squamous cell carcinomas with special emphasis on the topological distribution in the tumour. This was done in order to evaluate in squamous cell carcinoma a particular expression pattern observed recently by us in transitional cell carcinoma of the urinary tract and designated as an ‘interface phenomenon’;. This phenomenon implying maximum expression of cytokeratins 8 and 18 at the tumour front, and to a lesser extent also in areas of intratumorous stroma contact, was also found in about 50 per cent of the squamous cell carcinomas examined. It was even found for vimentin, which contrasted with transitional cell carcinoma. The percentages of occurrence of the phenomenon varied for the different sites of origin of the tumour. Tumour grade did not influence the results. These findings further support the idea that invasive carcinoma cells interacting with the stromal micro‐environment display a characteristic intermediate filament phenotype that deviates from the pattern expected on the basis of their direction of differentiation. These changes might eflect phenotype involved in invasive, migrating, and proliferating activities.
Intrahepatic distribution of transforming growth factor‐alpha (TGFα) during liver regeneration following carbon tetrachlorideinduced necrosis
Authors: Burr Andrew W. , Carpenter Martyn R. , Hines Julie E. , Gullick William J. , Burt Alastair D. 
Published: June 2005

AbstractThe distribution of transforming growth factor‐alpha (TGFα) in rat liver during regeneration was studied immunohistochemically using two antibodies, one a polyclonal (26T) raised against a synthetic peptide corresponding to the 17 C‐terminal amino acids of the mature rat protein, and the other a monoclonal (Ab‐2) raised against recombinant human protein. In normal liver, immunoreactive TGFα was detected in perivenular hepatocytes using both antibodies. No sinusoidal cells were found to contain the peptide. In response to carbon tetrachloride (CCI4)‐induced necrosis, an initial increase in the intensity of immunoreactivity was noted at 24 h following exposure to the toxin. This coincided with the period immediately preceding the peak of hepatocyte proliferation; Ab‐2 immunoreactive cells outnumbered 26T‐positive cells. Thereafter there was a reduction in the number of TGFα‐positive cells, but by day 4 the level of immunoreactivity had returned to that of normal liver. Using bromodeoxyuridine labelling, spatial and temporal relationships between TGFα expression and cell proliferation were identified, supporting the concept that this peptide plays an important role in the in vivo regenerative response to hepatic injury via an autocrine mechanism.
Cellular and molecular aspects of hepatic fibrosis
Authors: Burt Alastair D. 
Published: June 2005

AbstractHepatic fibrosis, a consequence of most forms of chronic liver disease, is a dynamic process involving complex interactions between several cell types, the net result of which is accumulation of several distinct extracellular matrix (ECM) proteins. The resultant disruption of intrahepatic blood flow contributes to the development of portal hypertension. The effects, however, are not merely a space‐occupying phenomenon; by changing the composition of the ECM, fibrosis may also alter hepatocyte function via cellular integrins. The principal source of ECM proteins in normal and fibrotic liver is the perisinusoidal cells which lie in the space of Disse. The response of this cell population to acute and chronic liver injury has been studied in detail. Perisinusoidal cells proliferate and become activated following hepatocyte necrosis. This phenomenon is transient in acute injuries, but in chronic liver disease, continued activation is associated with phenotypic modulation of perisinusoidal cells to myofibroblasts. This process is mediated by various cytokines including TGF‐β and PDGF. Some of the growth factors involved are derived from activated Kupffer cells and there is evidence of a complex interplay between mediators; injured sinusoidal endothelial cells and platelets are possible additional sources. Accumulation of ECM proteins in fibrosis can be explained not only by increased synthesis, but also by decreased degradation. There is growing evidence that in fibrotic liver there is decreased interstitial collagenase activity. This is, at least in part, due to expression of a tissue inhibitor of metalloproteinase, TIMP‐1, by activated perisinusoidal cells.
Monoclonal antibody 4C7 recognizes an endothelial basement membrane component that is selectively expressed in capillaries of lymphoid follicles
Authors: Jaspars Lies H. , Van Linden Hans C. Der , Scheffer George L. , Scheper Rik J. , Meijer Chris J. L. M. 
Published: June 2005

AbstractIn order to define compartment‐related structures within the extracellular matrix of human lymphoid organs, monoclonal antibodies (MAbs) were generated by immunizing mice with stromal fragments of human tonsils. One MAb (4C7) was selected which recognized an endothelial basal membrane component that is selectively expressed in capillaries of lymphoid follicles. The epitope was also present in follicles within chronically inflamed synovial membrane and in a hyperplastic thymus of a patient with myasthenia gravis. B‐cell non‐Hodgkin's lymphomas with a follicular growth pattern expressed the antigen in neoplastic follicles, whereas diffuse growing lymphomas lacked the antigen. The restricted distribution pattern suggests involvement of the 4C7‐defined antigen in the organization of the follicular compartment within human lymphoid tissue.