Acquired enophthalmos with systemic lupus erythematosus.

Ocular involvement sometimes occurs with systemic lupus erythematosus (SLE) but enophthalmos with SLE is rare. We report a case of enophthalmos with SLE. A 25-year-old male was admitted for two weeks of fever, sore throat, arthralgia, chest pain and right arm weakness with pain. We diagnosed him with SLE with malar rash, arthritis, pleural effusion, proteinuria, leukopenia, positive antinuclear antibody, anti-dsDNA, and lupus anticoagulant. The patient was prescribed high-dose prednisolone and hydroxychloroquine 400 mg. One week after discharge, he complained about a sensation of a sunken right eye. CT showed right enophthalmos, a post-inflammatory change and chronic inflammation. Proteinuria increased to 3.8 g/day after the patient stopped taking prednisolone. Cyclophosphamide therapy was administered for three months without improvement. We decided to restart prednisolone and change cyclophosphamide to mycophenolate mofetil. Proteinuria decreased but enophthalmos remains as of this reporting.

2,4,5-Trimethoxyldalbergiquinol promotes osteoblastic differentiation and mineralization via the BMP and Wnt/ß-catenin pathway.

Dalbergia odorifera has been traditionally used as a medicine to treat many diseases. However, the role of 2,4,5-trimethoxyldalbergiquinol (TMDQ) isolated and extracted from D. odorifera in osteoblast function and the underlying molecular mechanisms remain poorly understood. The aim of this study was to investigate the effects and possible underlying mechanisms of TMDQ on osteoblastic differentiation of primary cultures of mouse osteoblasts as an in vitro assay system. TMDQ stimulated osteoblastic differentiation, as assessed by the alkaline phosphatase (ALP) activity, ALP staining, mineralized nodule formation, and the levels of mRNAs encoding the bone differentiation markers, including ALP, bone sialoprotein (BSP), osteopontin, and osteocalcin. TMDQ upregulated the expression of Bmp2 and Bmp4 genes, and increased the protein level of phospho-Smad1/5/8. Furthermore, TMDQ treatment showed the increased mRNA expression of Wnt ligands, phosphorylation of GSK3, and the expression of ß-catenin protein. The TMDQ-induced osteogenic effects were abolished by Wnt inhibitor, Dickkopf-1 (DKK1), and bone morphogenetic protein (BMP) antagonist, noggin. TMDQ-induced runt-related transcription factor 2 (Runx2) expression was attenuatted by noggin and DKK1. These data suggest that TMDQ acts through the activation of BMP, Wnt/ß-catenin, and Runx2 signaling to promote osteoblast differentiation, and we demonstrate that TMDQ could be a potential agent for the treatment of bone loss-associated diseases such as osteoporosis.

Loss of presenilin 2 is associated with increased iPLA2 activity and lung tumor development.

Presenilins are the enzymatic components of γ-secretase complex that cleaves amyloid precursor protein, Notch and ß-catenin, which has critical roles in the development of Alzheimer's disease and cancer cell growth. Therefore, in the present study, we studied the effects and mechanisms of PS2 knockout on lung cancer development and possible mechanisms as a key regulator of lung tumor development. We compared carcinogen-induced tumor growth between PS2 knockout mice and wild-type mice. PS2 knockout mice showed increased urethane (1 mg/g)-induced lung tumor incidence when compared with that of wild-type mice with decreased activity of γ-secretase in the lung tumor tissues. Consequently, iPLA2 activities in lung tumor tissues of PS2 knockout mice were much higher than in tumor tissues of wild-type mice. Furthermore, knockdown of PS2 using PS2 siRNA decreased γ-secretase activity with increased iPLA2 activity in the lung cancer cells (A549 and NCI-H460), leading to increased lung cancer cell growth. PS2 knockout mice and PS2 knockdown lung cancer cells showed increased DNA-binding activities of nuclear factor kappa-beta, signal transducer and activator of transcription 3 (STAT3) and AP-1 which are critical transcriptional factors of iPLA2 than those of PS2 wild-type mice and control lung cancer cells. Taken together, these results suggest that the loss of PS2 could have a critical role in lung tumor development through the upregulation of iPLA2 activity by reducing γ-secretase.

Three-dimensional architectural and structural analysis--a transition in concept and design from Delaire's cephalometric analysis.

The aim of this study was to present a systematic sequence for three-dimensional (3D) measurement and cephalometry, provide the norm data for computed tomography-based 3D architectural and structural cephalometric analysis, and validate the 3D data through comparison with Delaire's two-dimensional (2D) lateral cephalometric data for the same Korean adults. 2D and 3D cephalometric analyses were performed for 27 healthy subjects and the measurements of both analyses were then individually and comparatively analyzed. Essential diagnostic tools for 3D cephalometry with modified definitions of the points, planes, and measurements were set up based on a review of the conceptual differences between two and three dimensions. Some 2D and 3D analysis results were similar, though significant differences were found with regard to craniofacial angle (C1-F1), incisal axis angles, cranial base length (C2), and cranial height (C3). The discrepancy in C2 and C3 appeared to be directly related to the magnification of 2D cephalometric images. Considering measurement discrepancies between 2D and 3D Delaire's analyses due to differences in concept and design, 3D architectural and structural analysis needs to be conducted based on norms and a sound 3D basis for the sake of its accurate application and widespread adoption.

Placenta-derived mesenchymal stem cells improve memory dysfunction in an Aß1-42-infused mouse model of Alzheimer's disease.

Mesenchymal stem cells (MSCs) promote functional recoveries in pathological experimental models of central nervous system (CNS) and are currently being tested in clinical trials for neurological disorders, but preventive mechanisms of placenta-derived MSCs (PD-MSCs) for Alzheimer's disease are poorly understood. Herein, we investigated the inhibitory effect of PD-MSCs on neuronal cell death and memory impairment in Aß1-42-infused mice. After intracerebroventrical (ICV) infusion of Aß1-42 for 14 days, the cognitive function was assessed by the Morris water maze test and passive avoidance test. Our results showed that the transplantation of PD-MSCs into Aß1-42-infused mice significantly improved cognitive impairment, and behavioral changes attenuated the expression of APP, BACE1, and Aß, as well as the activity of ß-secretase and γ-secretase. In addition, the activation of glia cells and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were inhibited by the transplantation of PD-MSCs. Furthermore, we also found that PD-MSCs downregulated the release of inflammatory cytokines as well as prevented neuronal cell death and promoted neuronal cell differentiation from neuronal progenitor cells in Aß1-42-infused mice. These data indicate that PD-MSC mediates neuroprotection by regulating neuronal death, neurogenesis, glia cell activation in hippocampus, and altering cytokine expression, suggesting a close link between the therapeutic effects of MSCs and the damaged CNS in Alzheimer's disease.

Antitumor activity of IL-32ß through the activation of lymphocytes, and the inactivation of NF-κB and STAT3 signals.

Cytokine and activation of lymphocytes are critical for tumor growth. We investigated whether interleukin (IL)-32ß overexpression changes other cytokine levels and activates cytotoxic lymphocyte, and thus modify tumor growth. Herein, IL-32ß inhibited B16 melanoma growth in IL-32ß-overexpressing transgenic mice (IL-32ß mice), and downregulated the expressions of anti-apoptotic proteins (bcl-2, IAP, and XIAP) and cell growth regulatory proteins (Ki-67 antigen (Ki-67) and proliferating cell nuclear antigen (PCNA)), but upregulated the expressions of pro-apoptotic proteins (bax, cleaved caspase-3, and cleaved caspase-9). IL-32ß also inhibited colon and prostate tumor growth in athymic nude mice inoculated with IL-32ß-transfected SW620 colon or PC3 prostate cancer cells. The forced expression of IL-32ß also inhibited cell growth in cultured colon and prostate cancer cells, and these inhibitory effects were abolished by IL-32 small interfering RNA (siRNA). IL-10 levels were elevated, but IL-1ß, IL-6, and tumor necrosis factor-alpha (TNF-α) levels were reduced in the tumor tissues and spleens of IL-32ß mice, and athymic nude mice. The number of cytotoxic T (CD8(+)) and natural killer (NK) cells in tumor tissues, spleen, and blood was significantly elevated in IL-32ß mice and athymic nude mice inoculated with IL-32ß-transfected cancer cells. Constituted activated NF-κB and STAT3 levels were reduced in the tumor tissues of IL-32ß mice and athymic nude mice, as well as in IL-32ß-transfected cultured cancer cells. These findings suggest that IL-32ß inhibits tumor growth by increasing cytotoxic lymphocyte numbers, and by inactivating the NF-κB and STAT3 pathways through changing of cytokine levels in tumor tissues.

Visual pathway-related horizontal reference plane for three-dimensional craniofacial analysis.

OBJECTIVES: To construct three-dimensional (3D) horizontal reference planes based on visual pathway and to determine their stability and reliability by analyzing the structural patterns of normal and dysmorphology for 3D craniofacial analysis. SETTING AND SAMPLE POPULATION: Thirty-six subjects with maxillofacial dysmorphology and malocclusion, and eight normal controls. MATERIALS AND METHODS POPULATION: On the 3D computed tomographic images of the subjects, the visual pathway-based planes, including the orbital axis plane (OAP), visual axis plane (VAP), and the optical axis plane (OpAP), were constructed and evaluated. RESULTS: The OAP, but not the VAP and OpAP, showed the ideal relationship between the midsagittal and posterior maxillary plane, and properly described the different patterns of maxillofacial dysmorphology with craniofacial plane 1 of Delaire's analysis and the occlusal plane. CONCLUSIONS: The proposed visual pathway-related horizontal reference planes, and in particular the OAP, seem to correctly express the visual axis and the position of the head in natural head position and can be used as a horizontal reference plane for the 3D analysis of craniofacial dysmorphology and anthropology.

Impact of postprandial hypertriglyceridemia on vascular responses in patients with coronary artery disease: effects of ACE inhibitors and fibrates.

We analyzed vascular responses (endothelial function, oxidant stress) to postprandial hypertriglyceridemia (PHTG) in patients with coronary artery disease (CAD) to reveal potential therapeutical effects of angiotensin converting enzyme inhibition (ACE-I) and of lipid lowering (fibrate). The study population (n=39, mean age: 60 years) consisted of four groups, all of which had angiographically documented CAD. A high fat group (n=9) consumed a high fat meal, a low fat group (n=9) a low fat meal, and ACE-I (n=10) or fibrate (n=11) groups consumed a high fat meal plus lisinopril or fenofibrate. Serum triglycerides (TG) increased significantly 2 h after eating a test meal in all groups with the exception of the low fat group. In the high and low fat groups changes of serum TG were positively correlated (r=0.664, P<0.005) with changes of phorbol ester-activated leukocyte superoxide anion radical (O(2-.)) formation and were negatively correlated (r=-0.488, P<0.05) with flow-mediated brachial artery dilation (FMD). There was a negative correlation (r=-0.419, P=0.094) between FMD and changes of O(2-.) formation in the high and low fat groups. In the ACE-I and fibrate groups, O(2-.) formation decreased 2 h after eating a test meal (from 5.34+/-1.01 to 3.81+/-1.15 nmol/10(6)cells per min, P<0.01, and from 4.66+/-0.91 to 4.26+/-0.97 nmol/10(6)cells per min, P=0.374, respectively). However, endothelial function did not show any significant changes 2 h after eating a test meal in all groups. PHTG increases oxidant stress and further deteriorates endothelial function, even in patients with CAD. Both ACE-I and fibrates have an antioxidant effect but no acute beneficial effects in terms of endothelial function under conditions of PHTG in CAD patients.

The properties of the ultramicrocylindrical ionization chamber for small field used in stereotactic radiosurgery.

Accurate dosimetry of small-field photon beams tends to be difficult to perform due to the presence of lateral electronic disequilibrium and steep dose gradients. In stereotactic radiosurgery (SRS), small fields of 6-30 mm in diameter are used. Generally thermoluminescence dosimetry chips, Farmer, Thimble ion chamber, and film dosimetry are not adequate to measure dose in SRS beams. These techniques generally do not provide the required precision due to their energy dependence and/or poor resolution. It is necessary to construct a small, accurate detector with high spatial resolution for the small fields used in SRS. The ultramicrocylindrical ionization chamber (UCIC) with a gold wall of 2.2 mm in diameter and 4.0 mm in length has dual sensitive volumes of air (8.0 mm3) and borosilicate (2.6 mm3) cavity. Reproducibility, linearity, and radiation damage with respect to absorbed dose, beam profile of small beam, and independence of dose rate of the UCIC are tested by the dose measurements in high energy photon (5, 15 MV) and electron (9 MeV) beams. The UCIC with a unique supporting system in the polystyrene phantom is demonstrated to be a suitable detector for the dose measurements in a small beam size.

Anti-Vascular endothelial growth factor treatment augments tumor radiation response under normoxic or hypoxic conditions.

Recent studies in experimental animals have shown that combining antiangiogenic therapy with radiation can enhance tumor response. Whether this enhancement is mainly attributable to angiogenesis inhibition, endothelial cell radiosensitivity, tumor cell apoptosis, or a decrease in the number of hypoxic cells (improved oxygenation) is not known. We designed this study to discern the role of tumor oxygenation. We chose an anti-vascular endothelial growth factor (anti-VEGF) monoclonal antibody (mAb) which has a known target, human VEGF. We also measured interstitial fluid pressure (IFP) to test the hypothesis that the decreased vascular permeability induced by the anti-VEGF mAb can lower IFP. The effect of anti-VEGF mAb on vascular density, partial oxygen tension (pO2), and apoptosis was also measured. Athymic NCr/Sed nu/nu mice bearing 6-mm xenograft of the human glioblastoma multiforme (U87), or colon adenocarcinoma (LS174T) were treated with anti-VEGF mAb injected i.p. on alternate days for a total of six injections at a dosage of 100 microg/injection/mouse. For combined anti-VEGF and radiation, single radiation doses were given under normal blood flow (20 and 30 Gy) or clamped hypoxic conditions (30 and 40 Gy) 24 h after the sixth injection of mAb. The inhibition of the growth of U87 and LS174T tumors by the anti-VEGF mAb was associated with a significant reduction in tumor vascular density and a relatively small increase in the number of apoptotic cells. Compared with size-matched controls, IFP decreased by 74% in LS174T, and 73% in U87 in mice treated with anti-VEGF mAb. After antibody treatment PO2 increased significantly in U87, but did not change in LS174T tumors. Combined treatment induced in U87 tumors a tumor-growth delay (TGD) which was greater than additive; in LS174T except for the 40-Gy hypoxic group, the effect was only additive. In both U87 and LS174T the TGD induced by the antibody was independent of oxygen levels in the tumor at the time of radiation. The fact that the increase in TGD occurred under both normoxic and hypoxic conditions suggests that anti-VEGF mAb treatment can compensate for the resistance to radiation induced by hypoxia.

Anti-CD9 monoclonal antibody-stimulated invasion of endometrial cancer cell lines in vitro: possible inhibitory effect of CD9 in endometrial cancer invasion.

Cell surface marker CD9 has been reported to play a role in inhibiting trophoblastic cell invasion. Since the invasive properties of cancer cells may resemble those of trophoblasts, we decided to investigate the role of CD9 in the invasion of endometrial cancer cells. In normal human endometrium, CD9 was found to be constitutively expressed on epithelial cells, as reported previously. While epithelial cells of endometrial hyperplasia (n = 5) were also positive for the expression of CD9, endometrial adenocarcinomas (n = 15) showed reduced expression. In order to clarify the significance of this reduced CD9 expression in endometrial cancer, an in-vitro invasion assay system was used to assess the effect of anti-CD9 monoclonal antibody (mAb) on the invasive properties of endometrial cancer cell line. Anti-CD9 mAb significantly enhanced invasion of the RL95-2 and Ishikawa cell lines, without affecting cell proliferation. Since CD9 is associated with the integrin subunits beta(1), alpha(3) and alpha(6) in human endometrium, we investigated the functional relationship between CD9 and these integrins in the RL95-2 cell line. Monoclonal antibodies against the integrins beta(1), alpha(3) and alpha(6) inhibited RL95-2 cell invasion. However, anti-CD9 mAb continued to show a stimulatory effect on RL95-2 cell invasion after treatment with anti-integrin alpha(3) mAb. In contrast, the anti-CD9 mAb had no effect after treatment with the mAb for integrins alpha(6) and beta(1). These findings indicate that CD9 is involved in regulating the invasive properties of endometrial carcinoma cells and that this effect is partially mediated by integrin subunits alpha(6) and beta(1). Thus, CD9 appears to be involved in the prevention of endometrial cancer invasion.

CD9 is expressed on human endometrial epithelial cells in association with integrins alpha(6), alpha(3) and beta(1).

Recently we reported that CD9 is involved in the invasion of a trophoblast-like choriocarcinoma cell line, BeWo, probably through the regulation of integrin functions. Integrins have also been reported to be expressed in the human endometrium and it has been suggested that they play important roles in blastocyst implantation. This study used immunohistochemistry to investigate the expression of CD9 in the endometrium during the menstrual cycle. CD9 was found to be intensely expressed on the cell surface of the glandular epithelium throughout the menstrual cycle without any apparent differences in staining intensity. In addition, Western blotting analysis of the affinity-purified proteins confirmed that CD9 was associated with integrins beta(1), alpha(3) and alpha(6) in the human endometrium. Therefore it can be concluded that CD9, in association with integrins alpha(6), alpha(3) and beta(1), is a constitutive molecule of the endometrial glandular epithelium. These results also suggest that CD9 may be an important regulator of these integrins in the human endometrium.

Angiocentric lymphoma of the head and neck: patterns of systemic failure after radiation treatment.

PURPOSE: To investigate the patterns of systemic failure and the clinical outcome in patients with angiocentric lymphoma of the head and neck who were treated with radiation alone, and to discuss the optimal mode of treatment for these patients. PATIENTS AND METHODS: We reviewed the records of 92 patients with stage I or II angiocentric lymphoma who were treated at Yonsei Cancer Center between 1976 and 1994. All patients were treated with involved-field irradiation. Radiation doses ranged from 40 to 60 Gy (median dose, 50.4 Gy). Treatment response, patterns of treatment failure including systemic failure, and clinical outcome after radiation treatment were analyzed. RESULTS: The most frequently involved site was the nasal cavity, either alone or in conjunction with other sites. In 16 patients (17.4%), angiocentric lymphoma was accompanied by cervical lymphadenopathy. Disease was classified as stage I in 62 patients (67.4%) and stage II in 30 patients (32.6%). After completion of radiation treatment, 61 patients (66.3%) achieved a complete response and 16 (17.4%) a partial response. Half of the patients (50.0%) ultimately experienced local recurrence with or without other components of failure, whereas regional failure was relatively uncommon (10.9%). Systemic failure occurred in 25.0% of patients during follow-up. Six patients had histologic findings identical to those at the time of the original disease (group I), whereas four patients exhibited morphologic features of frank lymphomas (group II). The majority of patients with systemic relapse had the predilection sites for widespread extranodal involvement, such as the skin, brain, lung, gastrointestinal tract, or testes. In addition, seven patients died from various medical illnesses or immunologic disorders, including hemophagocytic syndrome and second primary cancers (group III). After a median follow-up of 56 months, the overall survival and disease-free survival rates for all patients were 40.1% and 37.8%, respectively. All patients except one with systemic failure died within 1 year. CONCLUSION: Treatment with radiation alone had suboptimal results, partly because of the occurrence of a variety of systemic failure with diverse clinicopathologic features. Given the frequent occurrence of systemic failure after radiation treatment, we believe that the multimodality treatment approach containing more effective chemotherapeutic agents should be incorporated in the treatment of angiocentric lymphoma confined to the head and neck.

[A bibliographic study on Tongui-bigan with a special reference to its influence on Japan and China].

In this work my main focus was put on two things; first, to examine the history of publication of Tongui - bogam within the nation with particular interest in the changing aspect observed from the bibliographical terms, and second, to examine the process through which Tongui - bogam was introduced to Japan and China, and the influence the book brought the two nations. Some of the findings concerning the domestic publication of Tongui - bogam are as follows. The first printing of the book was made in 1613, under the auspice of Naeui - won, one of the government organs in the capital in charge of medical affairs. It was printed with wooden movable type carved at Hullyeon - togam, the military training bureau. As for the question of the history of the domestic publication of Tongui - bogam after the first printing in 1613, we don't have enough data yet. Although there are many different editions of Tongui - bogam extant today, with different size and different font each, I could find so far only three copies which carry the data concerning its publication, one printed in 1659 by the Kyongsang provincial government with newly engraved woodblock, one printed in 1754 again by the Kyongsang provincial government with re-engraved woodblock, and one printed in 1814 by the Cholla provincial government with newly re-engraved woodblock. Each of the three was a revised edition at the time of its publication because every time it was based on the copy corrected by Naeui - won. In addition to the above mentioned three different editions of Tongui - bogam, three are quite a few copies originally printed with wooden movable type of different font, at various time and various places. None of them has any record concerning the date and place of its publication, and none of them shows that it was based on the Naeui-won corrected version as a mother copy. Accordingly, all of them carry quite a few erratum misprinting and it seems quite certain that all of them were produced before 1659. I also feel that the 1724 Japanese edition was based on one of the pre - 1659 copies. In Japan, the first publication of Tongui - bogam was made in the year of 1724 (the 9th year of Kyoho in Japanese year title) under the auspice of the Japanese government i.e. the Tokugawa Bakuf. The book carries a preface written by a man named Fubihara, then the vice president of national university, and a postscript written by Minamoto mototoru, a government attached monk physician. It was a woodblock printing and the title of the book was "Kankoku - Teisei Tongui - bogam. The reason the word "Kankoku-Teisei" the Revised Edition Printed with Officially Engraved Woodblocks", was added to the title was that the publication was made by the government and before publication the government ordered Minamoto to read through the original Tongui-bogam throughly and make corrections if any misprintings be found. Minamoto also put the so-called kunto marks, the Japanese way of punctuation system on the original text all the way so that they could read it in the their own way. As the question of what edition of Tongi - bogam the Japanese used as a mother copy and whwn and how the mother copy had been brought to Japan are not clear at all. But judging from the fact that it carries quite a few erratum in spite of their efforts at proofreading before engraving the woodblock, it seems likely that Tongui - bogam they used as a mother copy was the one which was printed in Korea before 1659. In 1659 Tongui-bogam was published in Korea by the Kyongsang provincial government in Taegu with newly engraved woodblock. According to the attached record concerning its publication, it was a revised edition based on the Naeui - won corrected-copy, and this edition carries no misprintings in it at all. On the other hand, among the various editions of the extant Tongui - bogam today we can find some copy which, originally printed from wooden movable type, carries almost the same misprinting as those found in the 1724 Japanese edition. In other words, we are quite certain that the mother copy of the 1724 Japanese edition was brought to Japan before the Naeui - won - corrected - edition began to appear in Korea in 1659. The second publication of Tongui - bogam in Japan was made in 1799 in the city of Osaka. It was reprinted from the original woodblock of 1724 edition, and this second edition was later used in China in 1890 as a mother copy. The first publication of Tongui - bogam in China was made in the year 1766. It was a woodblock edition printed in Kwangtung province, located in the southern end of China. According to the attached preface written by a high ranking official named Nungo, a native of Kwangtung area, the publication was originally initiated by the governor of that province Mr. Wang, who deeply admired the value of Tongui - bogam. Since the Tongui - bogam at that time was available only in Bigak, the palace library in Peijing, the capital of the Ch'ing dynasty, the governor Mr. Wang had to send a man to Peijing to make a manuscript copy of Tongui - bogam of 25 of the volumes. But unfortunately Mr. Wang left his post before his plan to publish the book was realized and it was thanks to another native man named Chwahanmun who donated big money to cover the expenses of publication. The 1766 edition of Tongui - bogam, one copy of which is now in the possession of Kyungbuk University library, is understandably not a good copy, because it has many erratum in it. But it was reprinted afterwards sometimes with re-engraved woodblock many times at various places in China. The second publication of Tongui - bogam in China appeared in 1890. It carries a preface written by Mincheyusang. It was based on the Japanese edition printed in 1799 in Oosaka. What is interesting with Mr. Min's preface is that it shows their deep admiration of the value of Tongui - bogam on one hand, and at the same time very critical attitude toward the basic philosophy of Hojun on the other hand.

CD9 is involved in invasion of human trophoblast-like choriocarcinoma cell line, BeWo cells.

The CD9 molecule is expressed on human extravillous trophoblasts, which invade the endometrium during implantation and placentation. To elucidate the role of CD9 in trophoblastic function, we investigated the expression of CD9 protein and mRNA in BeWo cells, a human trophoblast-like choriocarcinoma cell line, using immunohistochemistry, Western blotting and reverse transcription-polymerase chain reaction (RT-PCR). When BeWo cells were cultured with anti-CD9 monoclonal antibodies (mAb), their invasion through the extracellular matrices was significantly enhanced in a dose-dependent manner. Cell proliferation and human chorionic gonadotrophin production were unaffected. On the other hand, culture in the presence of mAb against integrins alpha3, alpha5 and beta1, which partially block the interaction with the extracellular matrices, inhibited BeWo cell invasion. Anti-CD9 monoclonal antibody had a stimulatory effect on BeWo cell invasion in the presence of anti-integrin alpha3 antibody. In contrast, it had no effect in the presence of mAb against integrins alpha5 and beta1, which were also highly expressed on BeWo cells. These findings suggest that CD9 has a function connected with the invasive properties of BeWo cells, which is partially mediated by integrin alpha5beta1. This may relate to the involvement of CD9 in trophoblastic invasion.

Cyclic AMP receptor protein and TyrR are required for acid pH and anaerobic induction of hyaB and aniC in Salmonella typhimurium.

Two acid-inducible genes, aniC and aciK, that require anaerobiosis and tyrosine for expression were identified as orf326a encoding a potential amino acid/polyamine antiporter and hyaB encoding hydrogenase I, respectively. Cyclic AMP (cAMP) receptor protein, cAMP, and TyrR, regulator of aromatic amino acid metabolism, were strong positive regulators of both genes.

Improvement of X-ray beam quality for treating cancer using double focus electric field strings.

Accurate knowledge of the distribution and amount of contamination electrons arising from the gantry head at the surface and in the first few centimeters of tissue is essential for the clinical practice of radiation oncology. These electrons tend to increase the surface dose and deteriorate the buildup in the radiation field compared with a pure photon field. In this study, the relative quantity and reduction of contamination electrons in a therapeutic radiation photon beam (15 MV) was investigated. The contamination electrons can be separated out by a special device. This device, consisting of a double-focus electric field (8 x 10(5) V/m) made by a large number of strings 2 x 10(-4) m in diameter, removes contamination electrons and positrons without affecting the photon beam. It is located under the tray holder. In clinical practice, the device can decrease the relative surface charge and relative surface dose due to contamination electrons in the photon beam used in radiation therapy.

The utility of acoustic reflex thresholds and other conventional audiologic tests for monitoring cisplatin ototoxicity in the pediatric population.

OBJECTIVE: The sensitivity of acoustic reflex threshold changes for monitoring cisplatin ototoxicity in children was compared with the sensitivity of conventional audiometric tests. DESIGN: Acoustic reflex thresholds, thresholds for audiometric frequencies 0.250 Hz to 2 kHz and 3 kHz to 8 kHz, extended high-frequency (EHF) audiometry for 10 kHz to 16 kHz, and the articulation index (AI) were compared at six different cumulative dosage levels of cisplatin in 21 children, 3.08 yr to 19.25 yr of age. RESULTS: Of these 21 patients, 100% showed significant changes in at least one portion of the test battery when cumulative dosages exceeded 401 mg/m2. EHF testing was found to be the most sensitive to ototoxicity once cumulative dosage levels of 150 to 250 mg/m2 were reached. Audiometric thresholds from 3 to 8 kHz, and acoustic reflex threshold changes were found to be the next most sensitive to ototoxicity at cumulative dosages of 251 to 400 mg/m2. No significant threshold changes were noted for frequencies from 250 Hz to 2 kHz. CONCLUSIONS: Acoustic reflex threshold measures may prove to be a valuable addition to current ototoxic test protocols. Although it is currently not the most sensitive test to ototoxicity, it is one of the more objective tests. Further data must be collected to determine the clinical utility of acoustic reflex threshold testing to monitor ototoxicity.

[Clinical significance of serum CA130 level in women with spontaneous abortion, hydatidiform mole and early normal and tubal pregnancy].

We examined the serum CA130 level in women in early pregnancy with normal (n = 13), and abnormal (n = 28) course. The abnormal course consisted of intrauterine spontaneous abortion (n = 10), hydatidiform mole (n = 3) and tubal pregnancy (n = 15). The serum CA130 level was higher than for normal nonpregnant women (35u/ml) in 69% (9/13) of women with normal pregnancy, 90% (9/10) of those with intrauterine spontaneous abortion and 100% (3/3) of those with hydatidiform mole; the mean value and standard deviation for these three groups were 131 +/- 150u/ml (n = 13), 197 +/- 253u/ml (n = 10), and 47 +/- 15u/ml (n = 3), respectively. In contrast, the serum CA130 level of the 15 women with tubal pregnancy was 28 +/- 21u/ml. Among these patients, all of the 13 women without genital bleeding had a CA130 level within the normal range for nonpregnant women (mean +/- SD; 20 +/- 6u/ml). Since CA130 is abundant in the decidual tissue but is scant in tubal tissue, a high CA130 level in maternal sera during early pregnancy may indicate the presence of the destruction of decidual tissue, while a low or normal CA130 level throughout early pregnancy is regarded as characteristic of tubal pregnancy.