bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ultrastructural study of tumor cell differentiation in osteosarcoma of jaw bones*
Authors: Schulz A. , Maerker R. , Delling G. 
Published: April 2006

Abstract Two ostcosarcomas of jaw bones have been studied by electron microscopy. The objectives were to examine the specific cell types in relation to functions and ultrastructural features, and to examine matrices produced by tumor cells.The osteosarcoma cells were subdivided into four cell types: anaplastic, chondroblastic, osteoblastic, and ostcocytic–giant cells were not considered in the present investigation.Compared to normal bone cells, no specific sign of malignancy was found. However, tumor cells seem to lose functional abilities, i.e. a modification of matrix. Consequently, tumor matrix has altered organic and inorganic components with impairment of collagen maturation and matrix mineralization. The alteration in both processes may be related to a diminished production of proteoglycans.The cytogenic hypothesis of a tumor stem cell may be supported by the identification of anaplastic osteosarcoma cells resembling immature reticulum cells. One may speculate on transformation of this cell type as a genetically predetermined osteoprogenitor cell of malignant potential.
The immunopathogenesis of progressive chronic inflammatory periodontal disease
Authors: Seymour Gregory J. , Powell R. N. , Davies W. I. R. 
Published: April 2006

Abstract. Natural, humoral and cellular immune mechanisms have all been implicated in the pathogenesis of chronic inflammatory periodontal disease. However, confusion still exists as to the role played by each of these immunological mechanisms. Recently, characterization of the cell types within the progressive lesion has been established, in which four recognizable zones were described.Immediately subjacent to the epithelium lining the periodontal pocket both polymorphonuclear leukocytes (PMN's) and macrophages were seen, while cells deeper in the tissues had the morphological appearance of lymphocytes. The majority of these lymphocytes had a B‐cell phenotype although a few T‐cells and macrophages were found. On the advancing front of the lesion the cells had the morphological appearance of plasma cells, the majority of which contained IgG. Other cells found in this region had the morphology of plasma cells yet contained no cytoplasmic immunoglobulin, but they did contain substantial amounts of lysosomal enzymes. Similar cells have previously been described in periodontal disease; their frequent association with fibroblasts may suggest that they are important in the pathogenesis. Deposits of IgG and fibrin were found in the fibrous tissue band surrounding the lesion. These results are reviewed and, although the zones described were not anatomically distinct, by describing the lesion in this way it was possible to establish a convenient model to explain the immunopathogenesis of progressive chronic inflammatory periodontal disease. In this respect, progressive chronic inflammatory periodontal disease in man should be considered as a B‐cell lesion.
Dentinogenesis imperfecta: evidence of qualitative alteration in the organic dentin matrix
Authors: Takagi Y. , Koshiba H. , Kimura O. , Kuboki Y. , Sasaki S. 
Published: April 2006

Abstract Deciduous teeth affected by dentinogenesis imperfecta were obtained from two patients with osteogenesis imperfecta. Electronmicroscopy of the dentin revealed some structural alterations. The striation of the collagen fibrils was not clear, and the crystals were less dense than in normal dentin. The amino acid analysis of dentin collagen was slightly different from normal dentin. There were slight increases in the amounts of hydroxylysine. serine and acidic acids. On the other hand, lysine and arginine were reduced. The elevation of hexosyllysine content and an increase of carbohydrate were also observed.These results indicate that either dentin collagen is altered, or noncollagenous matrices associated with collagen are increased in dentinogenesis imperfecta dentin.
Detecting dentinal sclerosis in decalcified sections with the Pollak trichrome connective tissue stain
Authors: Stanley Harold R. , Broom Carol A. , Spiegel Eugene H. , Schultz Michael S. 
Published: April 2006

Abstract The supply of young human teeth for controlled human pulp studies is inadequate. Dentinal sclerosis in older teeth modifies the expected pulpal responses. Decalcification, necessary to interpret pulpal responses, destroys the primary evidence of sclerosis. At present we are unable to detect the degree of sclerosis and the pulp response in the same preparation. Valid interpretations on older teeth cannot be accomplished until this problem is resolved.Fifty‐seven teeth, normal and carious, representing a wide age span were fixed, embedded in Bioplastic and sectioned with the Bronwill Model #77 through the middle of the M‐D plane on the labio‐lingual plane to obtain an undecalcified ground section for examination with reflected and transmitted light and Faxitron 805 microradiography. The remaining portions of the tooth were decalcified, processed in paraffin and subjected to a variety of histochemical reactions including the Pollak trichrome slain. The Pollak trichrome and the Pollak trichrome solution #6 modification stains provided the greatest correlations with the sclerotic areas in the radiographs of the ground sections.Areas of dentin indicative of sclerosis prior to decalcification stained orange‐red with the Pollak trichrome stain and deep orange with the Pollak trichrome solution #6 modification.
Plasmacytoid myoepithelioma of the palate
Authors: Nesland Jahn M. , Olafsson Johannes , Sobrinho‐Simões Manuel 
Published: April 2006

We present the second case of plasmacytoid myoepithelioma of the palate, which was studied by light and electron microscopy. Apart from plasmacytoid cells, some spindle‐shaped cells were also observed. Both types of neoplastic cells had myoepithelial features, showing abundant 50–80 A thick filaments in the cytoplasm, and exhibited desmosomal junctions. A few light cells with less abundant filaments and better equipped with other organelles were observed.Our findings show that there is no clear‐cut distinction between the so‐called plasmacytoid myoepithelioma and the spindle and stellate myoepithelioma. We suggest that the ultrastructural appearance of these tumors together with the usual histological criteria for malignancy may be used to evaluate their prognosis.
Increased numbers of mast cells in the hyperplastic buccal mucosa of the zinc‐deficient rat
Authors: Kravich M. E. , Meyer J. , Waterhouse J. P. 
Published: April 2006

Abstract Six weanling male Sprague Dawley rats were fed a diet containing 0.4 ppm Zn and seven were fed an identical diet except for 40 ppm Zn. After 4 weeks, specimens of buccal mucosa in the region facing the molar teeth were removed. Paraffin sections, cut at 6 μ, were stained with toluidine blue, and tracings made of five sections per animal, spaced no less than 60 μm apart. Counts of mast cells over a measured length of section were made in a superficial zone of the lamina propria of 50 μm width and a deeper zone of 250 μ width.The average number of mast cells per mm in the subepithelial zone of the experimental animals was 15.4, the range 9.2–33.1. The control average was 4.0; the range was 2.9–5.3. No increase was found in the deeper zone.The epithelium was parakeratotic and its thickness was increased two‐fold. In the peripheral portion of the section, cellular and keratin layers were evenly increased in thickness, but in the central portion a disproportionate, nearly four‐fold increase occurred in the keratin layer and a lesser increase in the cellular layer.
Tumor antigens in neoplasms of the human parotid gland
Authors: Caselitz J. , Seifert G. , Jaup T. 
Published: April 2006

In a collection of parotid gland tumors the presence of different antigens was studied by immuno‐histochemical methods. The series was composed of different tumors: adeno‐ and cystadenocarcinomas, adenoid‐cystic carcinomas, salivary duct carcinomas, mucoepidermoid tumors, squamous cell carcinomas and anaplastic carcinomas.The following substances were studied:

Substances normally present in salivary glands like lysozyme and lactoferrin.
Oncofetal antigens: earcinoembryonic antigen (CEA) and alpha‐feloprotcin (AFP).
Different classes of intermediate‐sized filaments: prekeratin and vimentin. The presence of lactoferrin and carcinoembryonic antigen could be demonstrated in the glandular differentiated tumors, whereas the squamous cell carcinomas, although CEA positive, were lactoferrin negative. The anaplastic carcinomas were negative for lactoferrin and CEA. Lysozyme and AFP could not be demonstrated in the tumors of our material.

Mucoepidermoid tumors and squamous cell carcinomas were clearly positive for prekeratin filaments whereas the stromal part showed vimentin filaments in the cytoplasm of fibroblasls. These antigens provide a useful tool to distinguish between the epithelial and mesenchymal tumors.
Calcifying epithelial odontogenic tumors:
Authors: Ai‐Ru Liu , Zhen Liu , Jian Shao 
Published: April 2006

Nine cases of CEOT are reported. There are seven intra‐osseous and two extra‐osseous tumors. All but one occurred in the mandible. The age range was 20 to 64 years; averaging 34.2 years. There were 7 females and 2 males. Radiographically, they appeared either as monocystic or polycystic translucent lesions with radiopaque spots or masses. Embedded teeth were seen in six cases. Microscopically, four different patterns are described. No recurrence has been found post‐operatively within 2–14 years of follow‐up study.The nature of the reddish homogeneous material, the histogenesis of the tumor and the treatment are briefly discussed.
Epidermolysis bullosa
Authors: Wright J. T. , Gantt D. G. 
Published: April 2006

Epidermolysis bullosa (EB) describes a group of rare genetic mechanico‐bullous disorders. The disease has several modes of inheritance with various degrees of severity and expression. Two cases of recessive dystrophic EB are presented which show typical cutaneous, mucosal and occular involvement.The teeth were severely affected in both cases with much of the coronal enamel absent upon emergence into the oral cavity. The cervical enamel showed occasional hypoplastic pits. In one case, there was taurodontism of the permanent first molars. This case illustrates the increased occurrence of taurodontism associated with diseases affecting tissues of ectodermal origin. Taurodontism has not been previously reported with EB. Histologic studies of the teeth using light microscopy (LM) and scanning electron microscopy (SEM) revealed that the cementum and dentin were normal. The enamel, under LM, showed a prismatic structure with a broad neonatal line. SEM showed a wide amorphous zone of enamel adjacent to the dentin. Generalized throughout the enamel were globular areas within the prisms, which appeared to be local deformations. Hypoplastic pits on the surface were round and of varying diameters. The affected teeth exhibited both hypomaturation and hypo‐plastic defects of the enamel.
DNA flow cytometry of reclassified subtypes of malignant salivary gland tumors
Authors: Bang G. , Donath K. , Thoresen S. , Clausen O. P. F. 
Published: April 2006

Malignant salivary gland tumors are rare, constitute a heterogeneous group and are often difficult to diagnose histologically. This is borne out by the fact that in the present study 43.2% of 118 salivary gland tumors originally diagnosed as mucoepidermoid, acinic cell and adenoid cystic carcinomas had their original diagnosis altered upon reclassification. Patients with confirmed adenoid cystic carcinomas had a much worse prognosis than those with mucoepidermoid and acinic cell carcinomas.DNA flow cytometry showed that very few of the above mentioned three types of malignant neoplasms revealed aneuploid DNA stemlines, indicating that this is not a relevant prognostic tumor marker within the groups. However, several of the tumors that had their diagnosis changed, mostly to undifferentiated adenoor squamous cell carcinomas, showed aneuploid DNA stemlines. The survival time of patients with aneuploid tumors was considerably reduced compared to those with diploid tumors. Among confirmed acinic cell, mucoepidermoid and adenoid cystic carcinomas the S‐phase fraction was a significant prognostic factor, as it was among all tumors examined. This indicates that DNA aneuploidy and S‐phase fractions are potential prognostic factors for malignant salivary gland tumors, and that DNA flow cytometry may assist the characterization of such tumors.
Primary non‐Hodgin's lymphoma of the salivary glands. An analysis of 22 cases
Authors: Wolvius Eppo B. , van der Valk Paul , van der Wal Jacqueline E. , van Diest Paul J. , Huijgens Peter C. , van der Waal Isaäc , Snow Gordon B. 
Published: April 2006

Twenty‐two patients with primary non‐Hodgkin's lymphoma (P‐NHL) of the salivary glands have been studied with reference to age, sex, clinical symptoms, location of primary tumour, histological subtype, grade of malignancy according to the Working Formulation, stage of disease, treatment and follow up.The clinical features corresponded with previously reported data on salivary gland lymphomas. The most frequent histological diagnosis was MALT lymphoma. Most patients had a localised low‐grade lymphoma. Overall survival was influenced by grade of malignancy according to the Working Formulation.
The measurement of human pain
Authors: McGrath Patricia A. 
Published: April 2006

Abstract The assessment of human pain is complicated not only because pain, like other sensory experiences, is subjective, but also because pain, unlike other sensory experiences, may be modified by psychological, social, and situational factors. These factors can modify the neuronal response evoked by a relatively constant noxious stimulus (such as an injection) so that the resulting pain sensation may be enhanced or reduced. Consequently, in order to measure pain accurately, investigators must attempt to assess the subjective experience of pain.Although there are observational, self‐report, behavioral, and physiological methods available for measuring pain, direct scaling techniques may constitute a comprehensive measure by providing qualitative and quantitative estimates of pain expressed in terms of a patient's perception. A patient may rate both the strength and the affective dimensions of their clinical pain using simple measurement techniques that have been validated in well‐controlled studies on experimental pain. Direct scaling throughout a range of stimulus intensities (experimental pain) or throughout a range of time intervals (clinical pain) also provides a framework for standardization of individual responses. This standardization facilitates rigorous evaluation of analgesic efficacy for different pharmacological methods and for different pain conditions.The requirements for an objective measure of pain are similar to the requirements for any measuring instrument. These are: 1) reliability – that the procedure yields consistent results over time; 2) validity – that the procedure measures unequivocally a specific dimension of pain; 3) minimum inherent bias – that the procedure is relatively independent of method bias or patient/investigator response bias; and 4) versatility – that the procedure is applicable for both laboratory and clinical use and is practical for a wide variety of different medical settings.Visual analog scales, a direct scaling method in which a patient adjusts the length of a line so that the length is proportional to their pain, have been validated in a variety of experimental and clinical pain studies. Although these scales are deceptively simple, they have the reliability, validity, and versatility necessary for an objective pain measure.
Recommendations for evaluating agents for the reduction of dentinal hypersensitivity
Authors:   ADA Ad hoc Advisory Committee
Published: April 2006

*The following committee members were nominated by the Council on Dental Therapeutics and appointed by President Bentley: Dr. Major M. Ash, Jr., Professor and Chairman, Department of Occlusion, School of Dentistry, University of Michigan; Dr. Mohandas Bhat, Assistant Professor, Department of Community Dentistry, Case Western Reserve University; Dr. Nabil Bissada, Professor and Chairman, Department of Periodontics, School of Dentistry, Case Western Reserve University; Dr. Sebastian G. Ciancio, Professor and Chairman, Department of Periodontics, School of Dentistry, State University of New York at Buffalo; Dr. Louis P. Gangarosa, Professor and Coordinator of Pharmacology, School of Dentistry, Medical College of Georgia; Dr. Hans Graf, Chairman, Department of Periodontology, School of Dentistry, University of Bern (Switzerland); Dr. Isreal Klineberg, Chairman, Department of Oral Biology and Pathology, School of Dentistry, State University of New York at Stony Brook; Dr. Joseph A. Kanapka, Assistant Director, Dental Research, Vicks Research Center; Dr. Synguck Kim, Assistant Professor, Department of Endodontics, College of Dental and Oral Surgery, Colombia University; Dr. Walter T. McFall, Jr., Professor, Department of Periodontology, School of Dentistry, University of North Carolina; Dr. Patricia A. McGrath, Director, Pain Research Unit, Department of Oral Biology, Faculty of Dentistry, University of Western Ontario; Dr. David A. Pashley, Professor, Department of Oral Biology‐Physiology, School of Dentistry, Medical College of Georgia; Dr. Gerald Silverman, Private Practice, Hartford, Connecticut.Chairing the committee meeting were the following American Dental Association Staff Members: Dr. Kenneth H. Burrell, Assistant Secretary, Council on Dental Therapeutics; Dr. Conrad A. Naleway, Director, Division of Chemistry, Council on Dental Therapeutics; Dr. Helmut Zander, Special Consultant for Scientific Affairs, American Dental Association.The committee was funded by the American Fund for Dental Health through the support of the Block Drug Company, the John O. Butler Company, the Mentholaltim Company, and Richardson‐Vicks, Inc.
AMP-activated protein kinase protects against anti–epidermal growth factor receptor-Pseudomonas exotoxin A immunotoxin-induced MA11 breast cancer cell death
Authors: Andersson Yvonne , Le Hang , Juell Siri , Fodstad Øystein 
Published: April 2006

Abstract
We have shown previously that our 425.3PE immunotoxin inhibits protein synthesis and induces apoptosis in human breast cancer cells. In attempts to further elucidate the intracellular pathways implicated in its cellular effects, we found that the immunotoxin induced an initial stress response, which rapidly caused an imbalance in the cellular energy status with an increase in reactive oxygen species. The AMP-activated protein kinase (AMPK), a sensor of increased cellular AMP/ATP ratio, was activated by 425.3PE. An immunotoxin-induced activation of c-Jun NH2-terminal kinase (JNK) preceded and overlapped caspase-mediated cleavage of the α-subunit of AMPK in a time- and dose-dependent manner. The JNK activation occurred already at a dose level too low to induce any detectable changes in the apoptotic machinery or protein synthesis. In contrast, cycloheximide, even at a concentration causing a 90% inhibition of protein synthesis, did neither affect the ATP level nor activate JNK and AMPK. Pretreatment of the cells with the specific AMPK inhibitor compound C and JNK inhibitor SP600125 blocked activation of AMPK and JNK, respectively, and subsequently sensitized the cells to 425.3PE-induced cell death. Whereas the antioxidant N-acetyl-l-cysteine blocked the generation of reactive oxygen species and activation of JNK and AMPK, it did not block immunotoxin-induced apoptosis. Together, the results show that 425.3PE induces several parallel signaling events, observed initially as an early activation of survival pathways, protecting the cells against the toxic effects of the immunotoxin, followed by subsequent apoptosis induction and protein synthesis inhibition. Conceivably, therapeutic manipulation of the signaling intermediates AMPK and JNK might provide a means to maximize the anticancer effects of the 425.3 immunotoxin. [Mol Cancer Ther 2006;5(4):1050–9]
Organ-specific expression profiles of rat mammary gland, liver, and lung tissues treated with targretin, 9-cis retinoic acid, and 4-hydroxyphenylretinamide
Authors: Wang Yian , Yao Ruisheng , Maciag Anna , Grubbs Clinton J. , Lubet Ronald A. , You Ming 
Published: April 2006

Abstract
A rexinoid, targretin, and two retinoids, 9-cis retinoic acid (9cRA) and 4-hydroxyphenylretinamide (4HPR), were examined for their effects on gene expression in rat mammary gland, liver, and lung tissues. The chemopreventive effects of these agents have largely been attributed to their ability to interact with retinoic acid receptors (RAR) and/or retinoid X receptors (RXR). Targretin interacts with the RXR receptors. 9cRA interacts with both the RAR and RXR receptors, whereas 4HPR has a moderate affinity primarily for RAR γ. Based on previous studies on mammary chemoprevention, targretin (150 mg/kg diet), 9cRA (100 mg/kg diet), and 4HPR (782 mg/kg diet), were administered to rats continually in their diet for 7 days. Tissue- and agent-specific expression differences were determined by comparing tissues from treated rats with those from rats given a control diet. There were significantly more changes associated with targretin than 9cRA or 4HPR. Only a limited number of expression changes were found with 4HPR treatment. For each organ, targretin- and 9cRA-treated tissues clustered closely together, whereas 4HPR-treated tissues clustered with the tissues from the control diet group. In contrast to 9cRA treatment, targretin treatment altered genes that involved fatty acid metabolism and modulation of various cytochromes P450 in the liver, clearly demonstrating the very disparate nature of these two retinoids. These expression signatures could provide useful pharmacodynamic biomarkers for retinoid treatment and chemoprevention. [Mol Cancer Ther 2006;5(4):1060–72]
Targeted chemotherapy against intraperitoneally disseminated colon carcinoma using a cationized gelatin–conjugated HVJ envelope vector
Authors: Mima Hidetoshi , Yamamoto Seiji , Ito Makoto , Tomoshige Ryuji , Tabata Yasuhiko , Tamai Katsuto , Kaneda Yasufumi 
Published: April 2006

Abstract
The hemagglutinating virus of Japan envelope (HVJ-E; Sendai virus) vector derived from inactivated HVJ particles can be used to deliver DNA, proteins, and drugs into cells both in vitro and in vivo. HVJ-E is capable of delivering bleomycin, an anticancer drug, to various cancer cell lines, thereby producing 300-fold greater cytotoxicity than administration of bleomycin alone. In a mouse model of peritoneally disseminated colon cancer, we injected HVJ-E containing the luciferase gene into the peritoneum. Unexpectedly, luciferase gene expression was not observed within the tumor deposits or any organs. However, when combined with cationized gelatin (CG), CG-HVJ-E produced a high level of luciferase gene expression primarily within the tumor deposits. Forty-eight hours after introducing colon cancer cells into the peritoneum of experimental mice, CG-HVJ-E with or without bleomycin was injected into the abdominal cavity. Following six injections of bleomycin-incorporated CG-HVJ-E, complete responses were observed in 40% of the mice examined. All of the mice that received either empty CG-HVJ-E or bleomycin alone died within 40 days of having cancer cells introduced into the peritoneum. When the mice with complete responses were rechallenged with colon cancer cells from the same cell line, no tumors developed. Thus, CG-HVJ-E may suppress peritoneal dissemination of cancer. [Mol Cancer Ther 2006;5(4):1021–8]