Immunohistochemical analysis of transforming growth factor beta 3 expression in solitary morphoea profunda with histological membranocystic changes.
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Publications and source records attributed to T Baba.
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The present study determines the effect of surgical treatment of cardiovascular manifestations of Marfan syndrome in 72 patients by 114 operations, during 34-year period. This therapy resulted in aortic root repair, aortic arch replacement, or both in 78, mitral valve repair in 9, descending thoracic aortic replacement in 14, thoracoabdominal aortic replacement in 10, and abdominal aortic replacement in 6, including total aortic replacement in 4 and nearly total aortic replacement in 4 patients. Fusiform aneurysms were present in the the ascending aorta in 37, the aortic arch in 2, the thoracoabdominal aorta in 2, and the abdominal aorta in 6 patients. Aortic dissection occurred in 40 (55.6%), including type A aortic dissection in 29 patients. Aortic root repair included separate valve-graft in 8, Bentall composite valve-graft in 25, composite valve-graft with button technique in 26, composite valve-graft with interposition graft technique in 10, and valve sparing procedure in 5 patients. The overall early (30-day) mortality was 7.9%. The early survival was 75% in separate valve-graft procedure and 99.2% in composite valve-graft procedure. Late coronary dehiscence did not occur in the patients with Bentall technique in which the reattachments of coronary ostia were performed in 2 layers, but occurred in 50% of patients with the coronary anastomoses in 1 layer. Aortic valve regurgitation relapsed in 2 of the 5 patients with valve sparing procedure. Event free rate for the patients with composite valve-graft using button technique was 81.1% at 10 years. There were 14 late deaths; dissection or rupture of the residual aorta, composite graft endocarditis and cardiac failure were the principle causes of late deaths. In conclusion, Marfan patients with cardiovascular diseases can undergo surgical treatment with a low operative risk and low morbidity. Although late endocarditis remains a serious problem, we believe that Marfan syndrome is a contraindication for valve sparing procedure. Because of the potential for late dissection or aneurysm in other areas of the aorta, patients with Marfan syndrome should have serial computed tomographic scans indefinitely.
We cloned a novel ankyrin repeat protein, Arpp, by immunoscreening a cDNA library constructed from a human esophageal carcinoma cell line, TE1, with an antibody directed to a hypothetical protein encoded by antisense p53 mRNA. Arpp protein is composed of 333 amino acids and contains four ankyrin-like repeat motifs in the middle portion of the protein, a PEST-like sequence and a lysine-rich sequence similar to a nuclear localization signal in the N-terminal region, and a proline-rich region containing consensus phosphorylation sites in the C-terminal region. Protein sequence analysis revealed that Arpp is homologous (52.7% identity) to Carp which is shown to be involved in the regulation of the transcription of the cardiac ventricular myosin light chain 2 gene. Arpp mRNA was found to be expressed in normal skeletal and cardiac muscle. Interestingly, Arpp expression was detectable in bilateral ventricles, but undetectable in bilateral atria and large vessels, suggesting that Arpp may play a specific function in cardiac ventricles as well as skeletal muscles.
The aryl hydrocarbon receptor (AhR) repressor (AhRR) gene has been isolated and characterized from a mouse genomic library. The gene is distributed as 11 exons in a total length of about 60 kilobase pairs. Fluorescence in situ hybridization analysis has shown that the AhRR gene is located at mouse chromosome 13C2, at rat chromosome 1p11.2, and at human chromosome 5p15.3. The AhRR gene has a TATA-less promoter and several transcription start sites. In addition, putative regulatory DNA sequences such as xenobiotic responsive element (XRE), GC box, and NF-kappaB-binding sites have been identified in the 5'-upstream region of the AhRR gene. Transient transfection analyses of HeLa cells with reporter genes that contain deletions and point mutations in the AhRR promoter revealed that all three XREs mediated the inducible expression of the AhRR gene by 3-methylcholanthrene treatment, and furthermore, GC box sequences were indispensable for a high level of inducible expression and for constitutive expression. Moreover, by using gel mobility shift assays we were able to show that the AhR/Arnt heterodimer binds to the XREs with very low affinity, which is due to three varied nucleotides outside the XRE core sequence. We have also shown that Sp1 and Sp3 can bind to the GC boxes. Finally, both transient transfection analysis and gel mobility shift assay revealed that the AhRR gene is up-regulated by a p65/p50 heterodimer that binds to the NF-kappaB site when the cells has been exposed to 12-O-tetradecanoylphorbol-13-acetate, and this inducible expression was further enhanced by cotreatment of 12-O-tetradecanoylphorbol-13-acetate and 3-methylcholanthrene.
Monoclonal antibody (MAb) 1C5 reacts with 87% of uterine cervical adenocarcinoma and bovine beta -casein, but not with squamous cell carcinoma. To clarify the characteristics of the antigen (beta-casein-like protein; BCLP) recognized by MAb 1C5, molecular cloning was performed using 5' rapid amplification of the cDNA ends (5' RACE) and the oligo-capping method. The protein predicted from the cDNA consisting of 937 nucleotides comprises 222 amino acids. The BCLP gene and deduced amino acid sequences were novel and showed no similarity to known cancer-associated genes in the database. Northern blot analysis showed that a 1.1 kb transcript was ubiquitously expressed in cancer cell lines and was predominantly expressed in uterine cervical adenocarcinoma. To clarify the function of BCLP, BCLP cDNA was transfected into L929 cells, resulting in a significant increase in cell area, a downregulation of cell growth rate and a decrease in cell attachment. We conclude that BCLP might be associated with cell morphology and a regulation of growth pattern of tumor.
Both male and female beagle dogs (four dogs/sex) were orally treated with rifampicin (Rif) at the dose of 10 mg/kg/day for 7 days and an additional eight dogs (four dogs/sex) were used as a control. The inducible effect of Rif on intestinal cytochrome P450, especially CYP3A enzyme, was investigated by measuring microsomal testosterone 6beta-hydroxylation (6beta-OHT) activity, immunoblot and ELISA analysis. In male dogs, microsomal 6beta-OHT activity in the duodenum, upper, middle and lower part of the jejunum and the ileum of the control was 229, 204, 194, 129 and 57 pmol/min/mg protein, while the activity of the Rif-treated dogs significantly increased to 456, 486, 430, 192 and 138 pmol/min/mg protein, respectively. The activity of intestinal 6beta-OHT in the control and Rif-treated female dogs showed almost similar levels to those observed in the corresponding male dogs. The activity of intestinal 6beta-OHT in both control and Rif-treated dogs was specifically inhibited by anti-CYP3A12 antiserum. The apparent K(m) value for 6beta-OHT activity in all sections of the small intestine was comparable with that in the liver, and no significant changes were observed in between control and Rif-treated dogs. In both control and Rif-treated dogs, immunoblotting of intestinal microsomes with anti-CYP3A12 antiserum produced a band indistinguishable from that of purified CYP3A12 or of immunoreactive CYP3A12 in liver microsomes. A significant increase in intestinal CYP3A content by Rif treatment was quantitatively verified by the ELISA analysis and the magnitude of its increase correlated well with that of 6beta-OHT activity elevation. Furthermore, the results of immunohistochemistry using the anti-CYP3A12 antiserum indicated that CYP3A protein was specifically distributed in epithelial cells throughout the small intestine and appeared to be predominant at the apical side of villus cells. These results demonstrate that Rif induces not only hepatic CYP3A12 but also intestinal CYP3A in dogs.
The hiiragi (hrg) gene plays a key role in the development of the wing margin in Drosophila melanogaster. A mutation in the hrg gene resulted in a decrease in the level of the hrg transcript and was associated with a notched wing phenotype. We report here that the hrg gene encodes a poly(A) polymerase (PAP). The bovine cDNA for PAP type II reversed the phenotype due to mutation of the hrg gene, suggesting that hrg might encode a functional homolog of PAP. A mutation that reduced the enzymatic activity of Hrg failed to reverse the phenotype of hrg mutants, suggesting that the enzymatic activity of Hrg was required to rescue the wing phenotype. The levels of expression of wingless and cut at the presumptive wing margins were reduced in the late third-instar larvae of hrg mutants. These results suggest that the product of hrg is required for the normal expression of a series of genes in this region. Our results provide the first evidence that a PAP in Drosophila plays a key role in the early development of the wing margin, acting to regulate the specific expression of a series of genes via, perhaps, control of the processing of the 3' ends of transcripts.
BACKGROUND: Staphylococcus aureus is one of the major causes of community-acquired and hospital-acquired infections. It produces numerous toxins including superantigens that cause unique disease entities such as toxic-shock syndrome and staphylococcal scarlet fever, and has acquired resistance to practically all antibiotics. Whole genome analysis is a necessary step towards future development of countermeasures against this organism. METHODS: Whole genome sequences of two related S aureus strains (N315 and Mu50) were determined by shot-gun random sequencing. N315 is a meticillin-resistant S aureus (MRSA) strain isolated in 1982, and Mu50 is an MRSA strain with vancomycin resistance isolated in 1997. The open reading frames were identified by use of GAMBLER and GLIMMER programs, and annotation of each was done with a BLAST homology search, motif analysis, and protein localisation prediction. FINDINGS: The Staphylococcus genome was composed of a complex mixture of genes, many of which seem to have been acquired by lateral gene transfer. Most of the antibiotic resistance genes were carried either by plasmids or by mobile genetic elements including a unique resistance island. Three classes of new pathogenicity islands were identified in the genome: a toxic-shock-syndrome toxin island family, exotoxin islands, and enterotoxin islands. In the latter two pathogenicity islands, clusters of exotoxin and enterotoxin genes were found closely linked with other gene clusters encoding putative pathogenic factors. The analysis also identified 70 candidates for new virulence factors. INTERPRETATION: The remarkable ability of S aureus to acquire useful genes from various organisms was revealed through the observation of genome complexity and evidence of lateral gene transfer. Repeated duplication of genes encoding superantigens explains why S aureus is capable of infecting humans of diverse genetic backgrounds, eliciting severe immune reactions. Investigation of many newly identified gene products, including the 70 putative virulence factors, will greatly improve our understanding of the biology of staphylococci and the processes of infectious diseases caused by S aureus.
cDNA cloning and functional analysis of proacrosin from the ascidian Halocynthia roretzi were undertaken. The isolated cDNA of the ascidian preproacrosin consists of 2367 nucleotides, and an open reading frame encodes 505 amino acids, which corresponds to the molecular mass of 55,003 Da. The mRNA of proacrosin was found to be specifically expressed in the gonad by Northern blotting and in the spermatocytes or spermatids by in situ hybridization. The amino acid sequences around His(76), Asp(132), and Ser(227), which make up a catalytic triad, showed high homology to those of the trypsin family. Ascidian acrosin has paired basic residues (Lys(56)-His(57)) in the N-terminal region, which is one of the most characteristic features of mammalian acrosin. This region seems to play a key role in the binding of (pro)acrosin to the vitelline coat, because the peptide containing the paired basic residues, but not the peptide substituted with Ala, was capable of binding to the vitelline coat. Unlike mammalian proacrosin, ascidian proacrosin contains two CUB domains in the C-terminal region, in which CUB domain 1 seems to be involved in its binding to the vitelline coat. Four components of the vitelline coat that are capable of binding to CUB domain 1 in proacrosin were identified. In response to sperm activation, acrosin was released from sperm into the surrounding seawater, suggesting that ascidian acrosin plays a key role in sperm penetration through the coat. These results indicate that ascidian sperm contains a mammalian acrosin homologue, a multi-functional protein working in fertilization.
The appearance of serum troponin T (tn-T) on day 1 after acute myocardial infarction (AMI) strongly depends on coronary reperfusion. In contrast, the kinetics of tn-T release after day 1 after AMI are unaffected by the reperfusion status, and reflect the degradation of myofilaments in irreversibly damaged cells. However, it is not known whether serum tn-T levels after day 1 after AMI can be used to predict the long-term outcome. The purpose of this study was to elucidate the prognostic value of determining the tn-T level on day 3 or 4 after AMI. Serum tn-T levels on day 3 or 4 after AMI were measured in 121 patients (92 men and 29 women, mean age 65 years). Mean follow-up period was 526 days. There were 12 deaths (9 cardiac and 3 noncardiac) during the follow-up period. By Kaplan-Meier analysis, patients with tn-T levels higher than the median level (6.9 ng/ml) had a significantly higher mortality rate than those with submedian levels (p <0.01). By multivariate Cox proportional-hazards regression analysis, the serum tn-T level was an independent predictor of the long-term outcome after AMI (p <0.01). Futhermore, in patients with a first AMI, the serum tn-T level exhibited a significant negative linear correlation with left ventricular ejection fraction assessed 4 weeks after AMI (r = -0.48, p <0.001). Increased serum tn-T levels on day 3 or 4 after AMI are a powerful noninvasive predictor of poor long-term prognosis, reflecting residual left ventricular function after AMI.
Old problems, new ideas! The biomimetic phenol coupling of norbelladine derivatives such as 1 (Bn = benzyl) to form galanthamine (2), a drug used in the treatment of Alzheimer's disease, has been greatly improved by the use of the hypervalent-iodine oxidation reagent phenyliodine(III) bis(trifluoroacetate) (PIFA).
Since its establishment in 1991, the Rice Genome Research Program (RGP) has produced some basic tools for rice genome analysis, including a cDNA catalogue, a genetic linkage map and a yeast artificial chromosome (YAC)-based physical map. For the further development of rice genomics, RGP launched in 1998 an international collaborative project on rice genome sequencing. A P1-derived artificial chromosome (PAC)-based, sequence-ready physical map has been constructed using the PCR markers from cDNA sequences (expressed sequence tag [EST] markers). Selected PAC clones with 100-150 kb inserts from chromosomes 1 and 6 have been subjected to shotgun sequencing. The assembled genomic sequences, after predicting the gene-coding region, have been published both through a public database and through our website. As of January 2000, 1.9 Mb from 13 PAC clones were published. Future prospects for understanding rice genomic information at the nucleotide level are discussed.
Control sera are an essential component of in-vitro clinical diagnostic reagents. We have developed a control serum for HBsAg, anti-HCV, anti-HIV and anti- Treponema pallidum testing. Since this control serum is prepared from human plasma, we paid special attention to viral safety. We incorporated three viral inactivation methods into the manufacturing process that maintain the necessary characteristics of a stable control serum.
We present three cases of cervical spinal fracture, involving two columns without an obvious neurological deficit. Usually if two of three columns are fractured, the injury is considered unstable structurally and clinically. Fortunately our cases did not involve sensory or motor impairment because of an enlargement of the spinal canal.
Interstitial cells of Cajal (ICC) are responsible for generating electrical slow waves in the gastrointestinal (GI) tract. Slow waves regulate the frequency of contractions of the tunica muscularis, and therefore ICC are critical for normal motility in the small intestine. ICC express Kit, the gene product of c-kit, a protooncogene that encodes a receptor tyrosine kinase. Physiological evidence demonstrating that ICC are pacemakers has come from experiments on W-mutant mice which have few Kit-positive cells at the level of the myenteric plexus (IC-MY) and also lack electrical slow waves. In the past identification of ICC required the use of electron microscopy, however the discovery that ICC express Kit has facilitated studies of the distribution of ICC in several species. Immunoelectron microscopy to relate ultrastructure to Kit expression has only been performed in a limited number of studies of mice. We examined the ultrastructure of Kit-expressing cells in the rat using immunoelectron microscopy and an anti-Kit antibody. We compared the presence and appearance of Kit-expressing ICC in wildtype and Ws/Ws rats, which carry a mutation in the white spotting locus and have a phenotype similar to W/Wv mutant mice. Kit-expressing cells could be detected in the myenteric plexus (MY) and deep muscular plexus (DMP) regions of the small intestine of wildtype animals. In Ws/Ws rats, Kit-expressing cells were not observed in the region of MY, but were observed in the DMP. The density of Kit-positive cells in the DMP of Ws/Ws rats was similar to those in wildtype rats. Electron microscopy showed that Kit-expressing cells at the level of the MY of the rat had similar ultrastructural features as IC-MY in wildtype mice. IC-DMP in the rat of both wildtype and Ws/Ws mutants were similar in structure to IC-DMP of the mouse. We conclude that wildtype rats have IC-MY and IC-DMP in the tunica muscularis of the jejunum. ICC express Kit-like immunoreactivity (Kit-LI) in the rat as in the mouse. IC-MY are absent in the small intestine of Ws/Ws rats, and this corresponds to the lack of Kit-labeling in this region. Ws/Ws rats, however, possess IC-DMP with normal ultrastructural features and Kit-LI. The absence of IC-MY of Ws/Ws rats is likely to account for the abnormal contractile activity of the GI tract observed in these mutants. The present study suggests that Ws/Ws rats could provide an interesting model to investigate the physiological significance of pacemaker activity because they manifest a defect in IC-MY.
PURPOSE: To report same eye recurrence of acute retinal necrosis syndrome. METHODS: Two case reports. RESULTS: Acute retinal necrosis syndrome recurred in the left eye of a 60-year-old man 13 years after the initial episode, and recurred in the right eye of a 49-year-old woman 8 years after the initial episode. The recurrent necrotic lesions developed in normal appearing retina, unrelated to the location of the previous lesions. The recurrent lesions were successfully treated with acyclovir. CONCLUSION: Patients with acute retinal necrosis syndrome should be followed because of possible recurrence not only in the other eye but also in the same eye.
BACKGROUND: Small cerebral infarctions are common in elderly patients, but the association between the magnetic resonance imaging finding and neurologic dysfunction after coronary artery bypass grafting has not been evaluated. METHODS: We determined, prospectively, whether varying degrees of abnormal findings on magnetic resonance images of the brain increased the incidence of preoperative cognitive decline, postoperative neuropsychological dysfunction, and stroke in 421 elderly patients (> or = 60 years) undergoing coronary artery bypass grafting. RESULTS: Control patients (almost normal or leukoaraiosis, n = 212) had rates of postoperative neuropsychological dysfunction (7%) and stroke (1.4%); the small infarctions group (some small infarctions, n = 126) had rates of 13% and 5.6%, respectively; whereas patients with multiple infarctions (multiple small infarctions or broad infarctions, n = 83) had rates of 20% and 8.4%, respectively (p = 0.004, p = 0.013). In the group with multiple infarctions, 49 patients (59%) were asymptomatic and 21 patients (25%) had cognitive decline. Stepwise logistic regression analysis demonstrated that the significant predictors of multiple small infarctions or large infarctions were history of cerebrovascular disease, renal insufficiency, cognitive decline, and cerebral arteriosclerosis. CONCLUSIONS: Multiple infarctions significantly increase the risk of neurologic dysfunction after coronary artery bypass grafting. Routine screening for preoperative cognitive decline should be performed to detect underlying ischemic cerebral disease in elderly patients.