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We investigated the annealing effects of a magnetic tunnel junction on the Fe bottom pinned layer, of which the top surface was exposed to nitrogen plasma for a few tens of seconds prior to the deposition of the Al layer. The nitrogen-treated junction shows a lower magnetoresistance (MR) ratio and specific junction resistance (RA) than the untreated normal junction. However, after annealing at 230 °C, the MR ratio of the nitrogen-treated junction recovers to optimal values of the normal junction, while the RA remains lower than that of the normal junction. Furthermore, the nitrogen-treated junction shows less reduction of MR ratio and RA value with annealing at 270 °C for 3 h than the normal junction. From x-ray photoelectron spectroscopy and auger electron spectroscopy depth profiles, it is found that the nitrogen, which was initially at an interface between Al and Fe, diffuses into both the Al and FeMn layers after annealing at 230 °C. It seems that the nitrogen plays an important role in reducing Mn diffusion, as well as in improving the junction properties. © 2003 American Institute of Physics. [ABSTRACT FROM AUTHOR]

Aim: To evaluate the diagnostic role of additional oblique coronal and oblique sagittal magnetic resonance imaging (MRI) for an anterior cruciate ligament (ACL) tear., Materials and Methods: A total of 101 patients who had undergone preoperative knee MRI examinations with orthogonal and two sets of oblique images were enrolled in the study. Two radiologists evaluated the MRI images by the use of four methods: orthogonal images only (method A); orthogonal and additional oblique coronal images (method B); orthogonal and oblique sagittal images (method C); and orthogonal images with oblique coronal and sagittal images (method D). The status of the ACL (normal or tear) was determined by consensus. The sensitivity, specificity, and accuracy for an ACL tear with the use of each method were calculated in comparison with arthroscopy as the reference standard, and values were statistically analysed using the McNemar test. The diagnostic accuracies were compared using receiver operating characteristic (ROC) analysis., Results: Arthroscopy identified 10 partial ACL tears and 30 complete ACL tears. The specificities and accuracies for methods B, C, and D were significantly higher than the specificities and accuracies for method A (p<0.05). There was no significant difference in the sensitivity, specificity, and accuracy for methods B, C, and D. Diagnostic ability was not significantly different for each method, as determined by ROC analysis (p>0.05)., Conclusions: Additional oblique imaging for an ACL tear improved the specificity. Either of the oblique imaging methods is sufficient, and no further improvement in the diagnostic efficacy was achieved by simultaneous use.

The reduced incidence of cancer observed in schizophrenia patients may be related to differences in genetic background. It has been suggested that genetic predisposition towards schizophrenia is associated with reduced vulnerability to lung cancer, and p53 gene is one of the candidate genes. We tested the genetic association between schizophrenia and lung cancer by analyzing polymorphic sites in the p53 gene. Genotype and allele frequencies at two polymorphic sites in the p53 gene (BstUI and MspI restriction sites in exon 4 and intron 6, respectively) were studied in Korean schizophrenia (n=179) and lung cancer patients (n=104). Comparisons of the genotype and allele frequencies of the MspI polymorphism revealed significant differences between schizophrenia and lung cancer patients. The results suggest that the p53 polymorphism specifically found in schizophrenia patients may be associated with reduced vulnerability to lung cancer.

There are many mutations in the gene encoding Hepatitis B virus (HBV) core antigen of chronic active hepatitis patients, and such mutations are most likely to be related to the severity of disease. Here, we constructed plasmids containing wild-type and deletion type of HBV core gene (HBc) to develop an experimental DNA vaccine and to compare immunogenicity of two types of HBc vaccine. Twenty-nine wild-types and seven deletion types of HBc were detected in sera of 32 Korean patients with chronic active hepatitis. Four wild-types (W1, W2, W4, W6) and two deletion types (D3, D4) of HBc were cloned into the pcDNA3 vector. Intramuscular immunization with wild-type HBc efficiently increased serum anti-HBc antibody response in a dose-dependent manner. Anti-HBc antibody response in mice injected with W6 increased 14 days after immunization, and peaked after 30 days and was maintained at least up to 50 days. W6 immunization induced a specific cytotoxic T lymphocyte response to W6-transfected 3LL (3LL-W6), and reduced the sizes of tumor mass of mice challenged with 3LL-W6 or 3LL transfected with D4. However, intramuscular immunization with D3 and D4 did not show antibody response at all. D3 and D4 have 157 bp (from 331 to 491 bp) and 122 bp (from 327 to 448 bp) gene deletion, respectively, and these encode class II MHC-restricted T-cell epitope. Altogether, these results suggest that mutant virus that has deleted HBc gene may evade immune systems due to loss of T-cell epitope.

In the mammalian CNS, aspartate and glutamate are major excitatory amino acids, and their receptors are believed to mediate a wide range of physiological and pathological processes, including neurotransmission, plasticity, excitotoxicity, and various forms of neurodegeneration. The immediate early gene pip92 has been identified in serum-stimulated BALB/c 3T3 fibroblasts, activated T lymphocytes treated with cycloheximide, and fibroblast growth factor-stimulated hippocampal cells during neuronal differentiation. In this study we have demonstrated that pip92 is expressed in the mouse brain after a single intraperitoneal injection of NMDA. The distribution of pip92 mRNA levels in the NMDA-treated mouse brain was investigated using in situ RT-PCR. The region-specific activation of pip92 in the CNS was observed 3 h after NMDA injection, and high levels of pip92 mRNA were detected in the hippocampal dentate gyrus and piriform cortex regions. In addition, the activation of pip92 by NMDA was mediated by activation of mitogen-activated protein kinases (MAPKs), such as c-Jun N-terminal kinase (JNK) and p38 kinase, but not extracellular signal-regulated kinase (ERK) in the mouse hippocampus and immortalized rat hippocampal progenitor cells. This study suggests that pip92 is likely to play an important role in neuronal cell death induced by excitotoxic NMDA injury in the CNS.

Background and Purpose: Computerized 3-dimensional (3-D) motion measurement systems are used by those interested in human motion. The purposes of this study were (1) to determine the limits of accuracy in determining intersegmental angles during pendular motion at varying speeds and (2) to determine changes in accuracy introduced by autodigitization and digitization by experienced manual raters., Methods: Angular speed of a T-shaped pendulum was systematically increased by releasing the pendulum from 4 angles (0 degrees [no movement], 45 degrees, 90 degrees, and 120 degrees). Twelve reference angles calculated from markers placed on the pendulum were estimated over 20 frames for 10 trials at each release position., Results: Mean errors across trials and frames for intersegmental angles reconstructed by a 3-D motion measurement system were within +/- 1 degree across all release positions. An analysis of variance and a post hoc Tukey test revealed that the mean error for the autodigitized trials was larger than that for the manually digitized trials. For the autodigitized trials, the static trials (release position=0 degrees) produced less mean error than the trials with movement produced. The ICCs showed a high degree of consistency among all raters, ranging from .707 to .999., Conclusion and Discussion: Our findings support the conclusion that under carefully controlled conditions, a 3-D motion measurement system can produce clinically acceptable measurements of accuracy across a range of angular speeds. Furthermore, acceptable accuracy is possible regardless of the digitization method.

In order to develop an experimental DNA vaccine for the prevention and treatment of hepatitis B virus infection, hepatitis B virus surface antigen (HBsAg) DNA was subcloned into an E. coli-eukaryotic cell shuttle vector and was expressed in the Baculovirus expression system. Intramuscular, intradermal, and intraperitoneal injections of 30 microg of the plasmid DNA expressing HBsAg induced humoral and cellular immune responses in ICR mice. The first IgG antibodies were detected after ten days and specific IgG antibody titers peaked after two months of a single intramuscular DNA injection. Anti-HBs antibody titers gradually increased and peaked at four months following intradermal DNA injection, and in case of intraperitoneal injection they peaked at seven months. Generation of HBs-specific helper T lymphocytes was also investigated through the production of interleukin-2 by T helper cells. Boosting effects of HBs DNA were investigated without much results. In general, DNA-mediated HBs immunization induced humoral and cellular immune responses in mice that appears to simulate immune responses in human during the course of HBV vaccination.

Synaptic reorganization plays a very important role in brain adaptations to environmental stimuli, diseases, and aging processes. The NMDA model of excitotoxic injury was used to investigate the long-term molecular changes in the surviving neural cells in the mouse hippocampus. We demonstrated that a single intraperitoneal injection of NMDA produces persistent expression of c-fos, c-jun, Fas, and Fas ligand (FasL) mRNA in the hippocampus for 5 months. To determine the cellular origin of those gene transcripts in our in vivo model, a glial cell line and primary fetal neuronal culture were used to investigate the inducibility of the c-fos, c-jun, Fas, and FasL mRNA by NMDA. Both c-fos and Fas mRNA expression was observed in the NMDA-treated glial or neuronal cultures; however, c-jun and FasL mRNA was undetectable in this study. In our in vivo model, mossy fiber sprouting and apoptosis were also observed up to 40 days after the NMDA injection. Therefore, we hypothesize that the observed long-term expression of c-fos, c-jun, Fas, and FasL mRNAs may reflect the ongoing synaptic reorganization.

CD44 is a glycoprotein expressed in a wide variety of cell types. Recently expression of some alternatively-spliced variants of CD44 transcripts (CD44v) has been suggested to play a potential role in tumor metastasis and the detection of CD44v containing exon 6 to 11 may be helpful for the diagnosis of cancers. Expressions of CD44v containing exon 6 to 11 were investigated in 20 human colorectal cancer samples, peripheral blood leukocytes isolated from colorectal cancer patients, and 4 colorectal cancer cell lines using reverse transcription-polymerase chain reaction and Southern blot analysis. The standard form of CD44 transcripts was expressed in all samples tested. CD44v containing exon 6 to 11 was expressed in 18 cases of colorectal cancers (sensitivity = 90%), 3 out of 4 cell lines, and one normal tissue (specificity = 95%). These results suggest that the expression of CD44v containing exon 6 to 11 can be regarded as tumor specific and that this marker may be helpful for the early diagnosis of colon cancers, if specimens from the early stage are available.

The possibility of altering the course of prostatic cancer by immunologic means requires a clear understanding of the host-tumor relationship in this disease. Available data suggest that prostatic tumors contain both prostate-specific and tumor-specific antigens, although evidence on the latter is still debatable. Patients with prostatic cancer often show nonspecific depression of their cell-mediated immunocompetence, as do patients with many other forms of cancer. The question of whether prostatic cancers are immunogenic; that is, whether they elicit a specific immunologic response, remains unanswered.

Immunologic specificity of the prostatic acid phosphatase (PAP) and the kinetics of the PAP-anti-PAP antibody interactions were studied in detail. Antigenic identity of electrophoretic isozymes of PAP was established in this study. Counterimmunoelectrophoretic assay, radioimmunoassay, and immunofluorescence technique were developed to detect PAP and PAP-synthesizing cells. These techniques were applied to the determination of serum PAP levels and to the identification of metastatic prostate cancer cells in biopsies.

The immunologic specificity of human prostatic acidphosphatase has been established by several previous investigations as well as in this study. An apparent exception to this specificity was observed--a case of pancreatic islet cell carcinoma metastasized to the liver produced acid phosphatase that was immunologically indistinguishable from the prostatic acid phosphatase. In this case, the possibility of prostatic involvement was convincingly ruled out by clinical follow-ups and by postmortem pathologic studies. Highly purified prostatic acid phosphatase and this tumor acid phosphatase exhibited very similar Km values and identical molecular weights. Immunochemical analysis of the two enzymes using antiprostatic acid phosphatase sera showed that enzymes are antigenically identical. The implications of our observation are discussed in relation to clinical application of immunoassays for prostatic phosphatase in the future and to the molecular basis of human acid phosphatase polymorphism.

Studies of acid phosphates produced by cell lines MA 160 and EB 33 demonstrated immunochemically their prostatic origin. MA 160 and EB 33, rather than being HeLa contaminants, may be hybrids of prostatic epithelial and HeLa cells or true prostatic cell lines with chromosomal changes common to all long-term cultivated cell lines.

This review discusses the molecular and cytokinetic aspects of cellular aging of human diploid fibroblasts. Despite a large amount of data, the basis of their limited life span has not been defined. A replicative defect in aging cells lies in the mechanism(s) that initiates DNA synthesis, and the control of this mechanism(s) is mediated through an alteration in the sythesis of specific RNA and protein molecules. Two major groups of hypotheses have been offered to explain these findings. The differentiation hypotheses are based on the concept of a 'biological clock', while error hypotheses presuppose defects in genetic transcription or translation.

We have (a) examined culture conditions for prostatic cells, (b) devised a procedure for the selective enrichment of epithelial cells, and (c) developed a way to identify prostatic epithelial cells by immunologic methods.

Monoclonal antibodies against human prostatic acid phosphatase (PAPase) were produced by immunization of human primary spleen cell cultures. Dissociated spleen cells were cultured for 5-8 days in the presence of 100 ng/ml of PAPase and pokeweed mitogen (1:5000). Following immunization, B cells were isolated and infected with Epstein-Barr virus (EBV). Two weeks after EBV-transformation, cells were fused with either mouse myeloma cells (SP2/OAg14) or human/mouse heteromyeloma cells (SHM-D33). Hybrid clones were screened for anti-PAPase production. In 7 independent immunizations, the average fusion frequency was 3.6 per 10(6) lymphocytes. 18-32% of the hybridomas produced anti-PAPase; approximately 75% of these secreted IgM and 25% secreted IgG. Antibody specificity was determined by immunoassay and immunohistological studies. The procedures described here may be suitable for the production of human monoclonal antibody of a useful specificity.

Evaluation of serum acid phosphatase by 3 immunochemical methods (radioimmunoassay, counterimmunoelectrophoresis and immunoenzymoassay) was done in 3 groups of patients. In 42 patients wit stage D prostatic carcinoma a comparison of serum acid phosphatase determination by colorimetric assay and the 3 immunochemical methods in samples obtained before and after initiation of therapy showed an excellent correlation among the assays. Presently, we see no advantage of the immunochemical methods over the colorimetric assay in this group of patients. Among 100 patients studied in a blind fashion to detect those with unsuspected prostatic carcinoma no such cases were found. In the last group of patients with localized prostatic carcinoma staged surgically by pelvic lymphadenectomy the only elevations of serum acid phosphatase were observed in patients with extraprostatic involvement.

To evaluate the reliability of bone marrow acid phosphatase in the staging of prostatic carcinoma we analyzed 50 bone marrow samples collected at random from the hematology service at this hospital. The samples were assayed for acid phosphatase content by a colorimetric method using sodium thymolphthalein monophosphate as a substrate and by 2 immunochemical assays developed at our laboratory (counter immunoelectrophoresis and radioimmunoassay). We found a high percentage (61 per cent) of falsely positive results in patients with various hematological diseases without evidence of prostatic carcinoma by the colorimetric evaluation. All of these patients except 1 had negative immunochemical assay. Until a specific assay for prostatic acid phosphatase is developed for clinical use we caution the use of a single elevation of bone marrow acid phosphatase as a parameter of metastatic disease.

Hybrid cell lines producing monoclonal antibodies against human prostatic acid phosphatase (E. C. 3.1.3.2) were prepared by the fusion of mouse myeloma cells with the spleen cells of BALB/c mice and Lewis rats immunized with prostatic acid phosphatase (PAP). Approximately 14% of the hybrid cell microcultures which produced specific antibodies were cloned, and 6 eventually yielded stable cell lines. The monoclonal antibodies produced by these 6 hybridomas were characterized for their isotypes, isoelectric points, concentrations and affinities. The specificity of these monoclonal antibodies was further investigated by radioimmunoassay and immunohistochemical methods. All of the 6 monoclonal antibodies exhibited strict specificity for prostatic acid phosphatase.