[Atypical mycobacteriosis].
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Acquired Immunodeficiency Syndrome↗
Biomedical subjects
T Mori
Publications and source records attributed to T Mori.
[Prospective study of pulmonary embolism after total hip or knee arthroplasty].
We investigated the incidence of pulmonary embolism after total hip or knee arthroplasty. Arterial pO2 while the patient was breathing room air was measured at pre-operative day and 5 post-operative day using a Blood Gas Analyzer. Selection of patients for perfusion/ventilation scan during this study was dependent on the results of arterial blood gas determination that was more than 10 mmHg depression Of arterial pO2 level after surgery. More than depression of that was occurred in 11 patients (17.7%). Eight of them (72.7%) detected abnormalities (V/Q mismatch) in perfusion/ventilation scan, and we diagnosed them PE. More than 70% of PE was detected by only estimating the pre and post-operative arterial pO2. It was concluded that the estimation of arterial pO2 (pre and post-operation) was useful for the detection of PE, and combining estimation of arterial pO2 with the clinical feature evaluation method, low-invasive diagnosis and rapid treatment should be possible.
Aged↗
[Surgery in cats and experimental methods].
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Anesthesia↗
[Cavernostomy and simultaneous removal of fungus ball of pulmonary aspergilloma].
Between 1991 and 2000, 21 patients (16 male and 5 female) underwent 28 cavernostomies for the treatment of pulmonary aspergilloma. The median age was 59.4 years (range 37-85 years). The mean %VC was 59.6 (range 30.4-91.2), and the mean FEV 1.0 was 1.51 ml (range 0.64-2.67 ml). The mean body mass index was 17.6 (range 12.7-23.2). The most common complaint was hemoptysis. The underlying lung disease was tuberculosis in 17 cases, atypical mycobacteriosis in 2, and unclassified in 2. All cases had been diagnosed as complex aspergilloma. The mean surgical duration was 136 minutes (range 85-203 min.) and the mean blood loss during surgery was 242 ml(range 5-810 ml). No death or major complications occurred in the postoperative course. During follow-up, 4 patients died of massive hemoptysis, cancer, respiratory failure or an unknown cause. Relapses of aspergilloma occurred in 9 patients (42.9%). Recavernostomy was performed safely on 5 patients. In conclusion, although the relapse rate of aspergilloma was high after cavernostomy, safe reoperations were performed. Cavernostomy is thus an effective treatment in high-risk patients.
Adult↗
Electrostatic interactions of androgens and progesterone derivatives with rainbow trout estrogen receptor.
In primary cultures of immature male rainbow trout (rt) hepatocytes, vitellogenin (Vg) gene expression is regulated by E(2) via the estrogen receptor (ER). However, steroids other than estrogens can also stimulate Vg gene expression. These steroids are hardly converted into E(2) during incubation and their stimulatory activity is completely inhibited by tamoxifen implying rtER involvement. These steroids have no or a slightly positive charge on the Connolly surface. In contrast, steroids that failed to stimulate Vg gene expression had a strong positive or negative charge around rings C and D due to polarization. The amino acid sequences of the ligand binding domains (LBD) of rtER and human ER alpha have 57.7% homology; only one amino acid differs in the presumed steroid binding site. We modeled the three-dimensional structure of the LBD of rtER using X-ray crystallographic data for hER alpha in order to investigate the fit (structural and electrostatic) between steroid and rtER. Two factors are essential for binding to rtER: (i) hydroxyl or carbonyl groups near C3 and C17 of the steroids (hydrophilic regions) that can form hydrogen bonds with His(489), Arg(359), and Glu(318), (ii) a hydrophobic steroid nucleus that interacts with a hydrophobic region of the rtER LBD through van der Waals forces. If polar functional groups are present, the hydrophobic interaction between steroid and the rtER LBD is considerably weakened.
Amino Acid Sequence↗
Expression and prognostic significance in lung cancer of human tumor-associated antigen RCAS1.
A new monoclonal antibody (MAb), 22-1-1, acts against a novel tumor-associated antigen (Ag) strongly expressed in human uterine cervical adenocarcinomas. A cDNA encoding the Ag recognized by the 22-1-1 MAb has been isolated and called RCAS1 (receptor-binding cancer antigen expressed on SiSo cells). RCAS1 can induce growth arrest and apoptosis in RCAS1 receptor-positive cells including T cells and natural killer cells in vitro. These results suggest that RCAS1 is involved in tumor escape from the immune system. Immunohistochemical analysis revealed the relationship between RCAS1 expression and clinicopathological variables (age, sex, smoking, histology, differentiation grade, pathological T factor, N factor and stage) and the prognostic significance of RCAS1 in 66 lung-cancer patients who underwent curative operations: 33 adenocarcinomas, 24 squamous-cell carcinomas, 3 large-cell carcinomas, 4 adenosquamous carcinomas and 2 small-cell carcinomas. Median follow-up period of 64 non-small-cell carcinomas (NSCLCs) was 67.4 months. RCAS1 was expressed in 74.2% of lung cancers. RCAS1 in NSCLC cases with advanced T factor or pathological stage or in poorly differentiated adenocarcinomas was highly expressed. Furthermore, RCAS1 expression inducing apoptosis of tumor-infiltrating lymphocytes was a significant prognostic factor in NSCLC (p<0.03).
Adenocarcinoma↗
Novel design of nonpeptide AVP V(2) receptor agonists: structural requirements for an agonist having 1-(4-aminobenzoyl)-2,3,4, 5-tetrahydro-1H-1-benzazepine as a template.
The discovery of a series of nonpeptide arginine vasopressin V(2) receptor agonists is described. After identifying the aniline derivative 8 as our lead compound from the metabolites of compound 7 that showed antidiuretic activity by po administration to Brattleboro rats, improvements in the in vitro potency involving evaluations of the structural requirements for agonist action and optimizing the structure of the benzoyl moiety have been intensively undertaken. These studies led to compounds 16g, 19a, and 23b,h,i that show potent agonist activity for the V(2) receptor.
Administration, Oral↗
Somatic mutations of LKB1 and beta-catenin genes in gastrointestinal polyps from patients with Peutz-Jeghers syndrome.
Peutz-Jeghers syndrome (PJS) is characterized by multiple gastrointestinal hamartomatous polyps, mucocutaneous melanin deposition, and increased risk of cancer, mainly in the gastrointestinal tract. We examined mutations of the LKB1, beta-catenin, APC, K-ras, and p53 genes in 27 gastrointestinal hamartomatous polyps from 10 patients in nine PJS families. Of these hamartomatous polyps, one intestinal polyp had an adenomatous lesion, and one gastric polyp contained adenomatous and carcinomatous lesions. Germ-line mutations of the LKB1 gene were detected in six PJS families. Somatic mutations of the LKB1 gene were found in 5 polyps, whereas loss of heterozygosity (LOH) at the LKB1 locus at 19p was seen in 14 other polyps. In adenomatous lesions microdissected from hamartomatous polyps, both beta-catenin mutation and 19p LOH were detected. Furthermore, a carcinomatous lesion in a gastric hamartomatous polyp was found to contain a mutation of the p53 gene and LOH at the p53 locus in addition to LOH at the LKB1 locus and a beta-catenin mutation. K-ras mutations were detected in a few polyps, whereas no APC mutation or 5q LOH was detected in hamartomatous polyps. These results suggest that gastrointestinal hamartomatous polyps in PJS patients develop through inactivation of the LKB1 gene by germ-line mutation plus somatic mutation or LOH of the unaffected LKB1 allele, and that additional mutations of the beta-catenin gene and p53 gene convert hamartomatous polyps into adenomatous and carcinomatous lesions.
AMP-Activated Protein Kinase Kinases↗
[The effect of hydrochrolothiazide on the patient of nephrogenic diabetes insipidus].
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Adult↗
Effects of mifepristone (RU486) treatment on the development of uterine adenomyosis induced by pituitary grafting in mice.
To evaluate the effects of mifepristone (RU486) on the development of uterine adenomyosis induced by pituitary grafting (PG), 3 groups of mice receiving pituitary grafts at 7 weeks of age were given RU486 in food (20 mg/kg chow) from 3-14 (RU486-3 group) or 10-14 (RU486-10 group) weeks of age, or were given no further treatment (PG control group), respectively. All the mice were killed at 14 weeks of age. The uterine weight was significantly decreased in both RU486-treated groups compared with the PG control group. The incidence of adenomyosis was also decreased significantly in both the RU486-3 group (0/10 mice) and RU486-10 group (2/10 mice) compared with the PG control group (7/9 mice). To look for vascular changes in the uterine tissues, which have been reported to be related to the development of adenomyosis, immunohistochemical staining of von Willebrand factor in the blood vessels was performed. The mean surface area and minor axis of blood vessels in the uterus were thereby found to be significantly decreased in the RU486-10 group compared to the PG control group. The results clearly indicated that RU486, a potent antiprogestin, could inhibit the genesis of uterine adenomyosis in mice, and at the same time caused shrinkage of the vascular system. As in humans, progesterone as well as the vascular system therefore appear to be important factors in the pathogenesis of uterine adenomyosis in this mouse model.
Adenomyoma↗
Biogenesis of nonspecific lipid transfer protein and sterol carrier protein x: studies using peroxisome assembly-defective pex cell mutants.
Nonspecific lipid transfer protein (nsLTP; also called sterol carrier protein 2) with a molecular mass of 13 kDa is synthesized as a larger 15-kDa precursor (pre-nsLTP) with an N-terminal 20-amino acid extension presequence, as well as with the peroxisome targeting signal type 1 (PTS1), Ala-Lys-Leu, at the C terminus. The precursor pre-nsLTP is processed to mature nsLTP by proteolytic removal of the presequence, most likely after being imported into peroxisomes. Sterol carrier protein x (SCPx), a 59-kDa branched-chain fatty acid thiolase of peroxisomes, contains the entire pre-nsLTP moiety at the C-terminal part and is converted to the 46-kDa form and nsLTP after the transport to peroxisomes. We investigated which of these two potential topogenic sequences functions in biogenesis of nsLTP and SCPx. Morphological and biochemical analyses, making use of Chinese hamster ovary cell pex mutants such as the PTS1 receptor-impaired pex5 and PTS2 import-defective pex7, as well as green fluorescent protein chimeras, revealed that both pre-nsLTP and SCPx are imported into peroxisomes by the Pex5p-mediated PTS1 pathway. Nearly half of the pre-nsLTP remains in the cytosol, as assessed by subcellular fractionation of the wild-type Chinese hamster ovary cells. In an in vitro binding assay, only mature nsLTP, but not pre-nsLTP, from the cell lysates interacted with the Pex5p. It is likely, therefore, that modulation of the C-terminal PTS1 by the presequence gives rise to cytoplasmic localization of pre-nsLTP.
Acetyl-CoA C-Acetyltransferase↗
Perfect switching of photoreactivity by acid: photochemical decarboxylation versus transesterification of mesityl cyclohexanecarboxylate
Mesityl cyclohexanecarboxylate has been photodecarboxylated upon excitation at 254 nm to form cyclohexylmesitylene in good yield in neutral acetonitrile solutions. In the presence of a catalytic amount of the acid and ethanol as a nucleophile, however, the same compound undergoes facile transesterification upon irradiation, affording its ethyl ester in almost quantitative yield.
Journal Article↗
Third group of neostriatofugal neurons: neurokinin B-producing neurons that send axons predominantly to the substantia innominata.
Neostriatal neurons that produce neurokinin B were investigated immunocytochemically in the rat brain with an antibody against the C-terminal portion of the precursor prepropeptide of neurokinin B, preprotachykinin B (PPTB). PPTB-immunoreactive neurons were scattered throughout the neostriatum and constituted 5.1% of neostriatal neurons. They were immunopositive for projection neuron markers, such as precursor peptides of substance P, enkephalins, and dynorphins, but negative for intrinsic neuron markers, suggesting that PPTB was expressed in neostriatal projection neurons. However, PPTB-immunoreactive neurons were immunonegative for dopamine- and cyclic AMP-regulated phosphoprotein, which is known to be produced by striatopallidal and striatonigral neurons. Furthermore, almost no PPTB-immunoreactive axon terminals were observed in the substantia nigra or globus pallidus. The authors then made large kainic acid lesions in the neostriatum to reveal the target areas of PPTB-producing neurons and observed a decrease in PPTB-immunoreactive fibers in the sublenticular portion of the substantia innominata and, to much lesser extent, in the bed nucleus of the stria terminalis and central nucleus of the amygdala. After injection of wheat germ agglutinin into the substantia innominata, PPTB immunoreactivity was detected in many retrogradely labeled neostriatal neurons. In contrast, no PPTB immunoreactivity was observed in striatonigral or striatopallidal neurons after injection of retrograde tracers into the substantia nigra or globus pallidus. Thus, neurokinin B-producing neostriatal neurons were considered to send projection fibers predominantly to the substantia innominata. Furthermore, PPTB-immunoreactive axonal swellings were closely apposed to neurokinin B receptor-immunoreactive dendrites in the substantia innominata. Overall, the present results indicate that the rat brain possesses a chemically and hodologically unique neostriatofugal pathway in addition to the direct and indirect pathways.
Animals↗
CD45 opposes beta-amyloid peptide-induced microglial activation via inhibition of p44/42 mitogen-activated protein kinase.
Reactive microglia have been suggested to play a role in the Alzheimer's disease (AD) process, and previous studies have shown that expression of CD45, a membrane-bound protein-tyrosine phosphatase (PTP), is elevated in microglia in AD brain compared with controls. To investigate the possible role of CD45 in microglial responsiveness to beta-amyloid (Abeta) peptides, we first co-treated primary cultured microglia with a tyrosine phosphatase inhibitor [potassium bisperoxo (1,10-phenanthroline) oxovanadate (phen), 5 micrometer] and freshly solubilized Abeta peptides (1000 nm). Data show synergistic induction of microglial activation as evidenced by tumor necrosis factor alpha (TNF-alpha) production and nitric oxide (NO) release, both of which we show to be dependent on activation of p44/42 mitogen-activated protein kinase (MAPK). Furthermore, co-treatment with phen and Abeta peptides results in microglia-induced neuronal cell injury. Stimulation of microglial CD45 by anti-CD45 antibody markedly inhibits these effects via inhibition of p44/42 MAPK, suggesting that CD45 is a negative regulator of microglial activation. Accordingly, primary cultured microglia from CD45-deficient mice demonstrate hyper-responsiveness to Abeta, as evidenced by TNF-alpha release, NO production, and neuronal injury after stimulation with Abeta peptides. As a validation of these findings in vivo, brains from a transgenic mouse model of AD [transgenic Swedish APP-overexpressing (Tg APP(sw)) mice] deficient for CD45 demonstrate markedly increased production of TNF-alpha compared with Tg APP(sw) mice. Taken together, these results suggest that therapeutic agents that stimulate the CD45 PTP signaling pathway may be effective in suppressing microglial activation associated with AD.
Alzheimer Disease↗
Cdk2-dependent phosphorylation and functional inactivation of the pRB-related p130 protein in pRB(-), p16INK4A(+) tumor cells.
The retinoblastoma family proteins pRB, p107, and p130 are phosphorylated and released from E2Fs in the late G(1) phase of the cell cycle. This phosphorylation is thought to contribute to the derepression of E2F-responsive genes and to be mediated, in part, by Cdk4 and Cdk6. Evidence that Cdk4/6 activity is inhibited by p16(INK4A) in most pRB(-) cells suggests that p107 and p130 may be underphosphorylated and remain associated with E2Fs during G(1)-S progression in cells that lack pRB. To examine this, we evaluated the cell cycle-dependent phosphorylation and E2F binding abilities of p107 and p130 in pRB(-), p16(+) Saos-2 osteosarcoma cells. p130, but not p107, was phosphorylated and released from E2F-4 in late G(1) and S phase cells, although p130 phosphorylation differed qualitatively in these and other pRB(-), p16(+) cells as compared with pRB(+), p16(-) cell types. p130 phosphorylation occurred in the absence of cyclin D-Cdk4/6 complexes, coincided with cyclin E- and Cdk2-associated kinase activity, and was prevented by expression of dominant negative Cdk2. Moreover, dominant negative Cdk2 prevented the dissociation of endogenous p130-E2F-4 complexes and inhibited E2F-4-dependent transcription. These findings show that p130 can be phosphorylated and functionally inactivated in a Cdk2-dependent process, and they highlight the involvement of distinct Cdks in the regulation of different pRB family proteins.
CDC2-CDC28 Kinases↗
p53AIP1, a potential mediator of p53-dependent apoptosis, and its regulation by Ser-46-phosphorylated p53.
Through direct cloning of p53 binding sequences from human genomic DNA, we have isolated a novel gene, designated p53AIP1 (p53-regulated Apoptosis-Inducing Protein 1), whose expression is inducible by wild-type p53. Ectopically expressed p53AIP1, which is localized within mitochondria, leads to apoptotic cell death through dissipation of mitochondrial A(psi)m. We have found that upon severe DNA damage, Ser-46 on p53 is phosphorylated and apoptosis is induced. In addition, substitution of Ser-46 inhibits the ability of p53 to induce apoptosis and selectively blocks expression of p53AIP1. Our results suggest that p53AIP1 is likely to play an important role in mediating p53-dependent apoptosis, and phosphorylation of Ser-46 regulates the transcriptional activation of this apoptosis-inducing gene.
Adenocarcinoma↗
A Case of Tuberculous Uveitis Complicated by Myelodysplastic Syndrome.
Background: Recently, the incidence of tuberculosis in compromised hosts has increased.Case: A 52-year-old man suffering from myelodysplastic syndrome (MDS) had pulmonary tuberculosis. On June 22, 1996, we found a disc-sized choroidal lesion with milky appearance on the paramacular in his right eye. After 1 month, a similar choroidal lesion was found near the disc in the same eye. In spite of chemotherapy for MDS and antituberculosis medications, those choroidal lesions gradually enlarged. In November, satellite lesions were found around them. Some retinal exudates and hemorrhage were also detected in both eyes. He died on April 6, 1997. We found Langhan's giant cells in the choroid on the specimen of his eyes. So we judged the choroidal lesions to be tuberculous uveitis.Conclusion: This case showed choroidal tuberculosis and choroidal miliary tuberculosis in the same eye that were resistant to medications. We thought resistance to medication was due to destruction of the immune system by MDS.
Journal Article↗
Anti-tumor immunity against CT26 colon tumor in mice immunized with plasmid DNA encoding beta-galactosidase fused to an envelope protein of endogenous retrovirus.
Endogenous retroviral gene products have been recognized as being expressed in human cancerous tissues. However, these products have not been shown to be antigenic targets for T-cells, possibly due to immune tolerance. Since carcinogen-induced colon tumor CT26 expresses an envelope protein, gp70, of an endogenous ecotropic murine leukemia virus that is comparable to human tumor-associated antigens, we examined whether a DNA vaccine containing the gp70 gene induces protective immunity against CT26 cells. Injection of mice with plasmid DNA (pDNA) encoding gp70 alone failed to induce anti-gp70 antibody (Ab) or anti-CT26 cytotoxic T lymphocyte (CTL) responses. However, immunization with pDNA encoding the beta-galactosidase (beta-gal)/gp70 fusion protein induced anti-gp70 Ab and anti-CT26 CTL responses and conferred protective immunity against CT26 cells. These results indicate that beta-gal acts as an immunogenic carrier protein that helps in the induction of immune responses against the poorly immunogenic gp70. Considering these results, it is possible that potential tolerance to the endogenous retroviral gene products expressed by human tumors may be overcome by DNA vaccines that contain an endogenous retroviral gene fused to genes encoding immunogenic carrier proteins.
Animals↗