Anesthetic management in obese parturients.
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Journal Article↗
Biomedical subjects
T Nishikawa
Publications and source records attributed to T Nishikawa.
New Prognostic Factors Associated with Long-term Survival in Node-Negative Breast Cancer Patients.
BACKGROUND: This study was undertaken to determine the absolute and relative value of angiogenesis, proliferating cell nuclear antigen (PCNA) and conventional prognostic factors in predicting relapse-free survival (RFS) and overall survival (OS) rates associated with long-term survival in Japanese patients with node-negative breast cancer. PATIENTS AND METHODS: Two hundred patients with histological node-negative breast cancer were studied. We investigated nine clinicopathological factors, including angiogenesis, PCNA using per-manent-section immunohistochemistry, clinicaltumor size, histological grade (HG), tumor necrosis, lymphatic vessel invasion (LVI), histological extension, histological classification, and infiltrating growth (INF), followed for a median of 10 years (range, 1 to 20). RESULTS: Twenty-one patients (10.5%) had recurrence and 15 patients (7.5%) died of breast cancer. Univariate analysis showed that PCNA, clinical tumor size, HG, angiogenesis, and LVI were significantly predictive of 20-year RFS or OS. Tumor necrosis was significantly predictive of OS, not of RFS. Multi-variate analysis showed that clinical tumor size (P = 0.0003), angiogenesis (P = 0.0003), PCNA (P = 0.0064), and HG (P = 0.0401) were significant independent prognostic factors for RFS. PCNA (P< 0.0001) and clinical tumor size (P = 0.0112) were significant independent prognostic factors for OS, while angiogenesis was a borderline significant factor. CONCLUSION: PCNA and angiogenesis were important new prognostic factors in node-negative breast cancer patients.
Journal Article↗
Stereocontrolled Synthesis of (-)-5,11-Dideoxytetrodotoxin.
New derivatives of an intriguing marine natural product are now accessible. The first asymmetric synthesis of the simple tetrodotoxin analogue, 5,11-dideoxytetrodotoxin (3), was achieved. Hydroxylation at position C8 of the key intermediate 1 relied on the neighboring trichloroacetamide group, and stereoselective elaboration of the vinyl group gave alpha-hydroxylactone 2, which was transformed into the title compound through a new guanidylation method.
Journal Article↗
A novel calcitonin receptor gene in human osteoclasts from normal bone marrow.
The calcitonin receptor (CTR) gene in human osteoclasts formed in a human bone marrow cell culture system was examined by reverse transcription-polymerase chain reaction (RT-PCR). The RT-PCR results indicated that the 5'-untranslated region (5'UTR) was different between CTR mRNAs in human osteoclasts and in a mammary tumor cell line, MCF-7 cells. We isolated the 5'UTR of the CTR gene from human osteoclasts, whose sequence had only 28.6% identity with that of other CTR genes reported until now. In a radioligand binding assay, COS-1 cells transfected with the osteoclast CTR gene bound to [125I]human CT (hCT). These results provided evidence that the CTR gene cloned from human osteoclasts was expressed functionally and its coding protein was identical to MCF-7 cell CTR.
5' Untranslated Regions↗
Reconstitution of active recombinant Shiga toxin (Stx)1 from recombinant Stx1-A and Stx1-B subunits independently produced by E. coli clones.
Escherichia coli clones expressing recombinant Shiga toxin (Stx)1-A and recombinant Stx1-B subunits, were established. Culture supernatants of these clones were examined for inhibitory activity on in vitro protein synthesis using luciferase as a reporter enzyme. Culture supernatant of the clone expressing Stx1-A, but not Stx1-B, showed the inhibitory activity. Neither recombinant Stx1-A nor Stx1-B showed Vero cell cytotoxicity. For reconstitution of biologically active toxin, the culture supernatants of the Stx1-A clone and the Stx1-B clone were mixed. The reconstituted recombinant Stx1 showed both Vero cell cytotoxicity and inhibition of in vitro protein synthesis.
Animals↗
Inhibitory effects of vesnarinone in the progression of myocardial damage in experimental autoimmune myocarditis in rats.
OBJECTIVES: Vesnarinone, a positive inotropic and immunomodulatory agent, diminishes nitric oxide (NO) levels by suppressing the induction of inducible NO synthase (iNOS) expressed in cytokine-stimulated macrophages and cardiomyocytes. We examined whether vesnarinone exerts inhibitory effects on the progression of myocardial damage in experimental autoimmune myocarditis in rats through suppression of iNOS. METHODS: Myocarditis was induced in 30 Lewis rats by injection of porcine cardiac myosin and vesnarinone was orally administered to 20 of the 30 rats. On day 21 after immunization (the climax of inflammation), the hemodynamics were examined and the severity of myocarditis was evaluated by determining the area ratio (%) [affected/entire area] of myocardial lesions in histological sections. Levels of serum CK-MB, NOx (NO2(-)+NO3-), TNF-alpha and IL-1 beta, and cyclic GMP, iNOS mRNA, TNF-alpha and IL-1 beta in heart tissues were determined. Expression of iNOS and TNF-alpha protein were examined by immunohistochemical methods. RESULTS: Histopathological examination revealed extensive myocardial destruction and massive infiltration of inflammatory cells in the vesnarinone-untreated rats. The area ratio of the lesions in the treated rats was significantly lower than that in the untreated ones. Levels of CK-MB, NOx, cyclic GMP, cytokines and iNOS mRNA were significantly lower in the vesnarinone-treated rats. Infiltrating macrophages and cardiomyocytes in the untreated rats showed much higher levels of expression of iNOS and TNF-alpha than those in the vesnarinone-treated rats. CONCLUSIONS: Vesnarinone may prove to be useful in the treatment of myocarditis by attenuating NO production through suppression of iNOS induced by cytokines.
Analysis of Variance↗
Study of a rat skin in vivo micronucleus test: data generated by mitomycin C and methyl methanesulfonate.
We have developed an in vivo micronucleus (MN) test that uses rat skin as the target organ. Sample preparation involves cold-treating the epidermis with trypsin, peeling it off with a fine forceps, treating it in hypotonic solution, and staining it with acridine orange (A.O.). We evaluated the assay using mitomycin C (MMC) and methyl methanesulfonate (MMS) as model clastogens, applying them as single and repeat treatments. Both chemicals induced a significant, dose-dependent increase in MN frequency in basal cells. One treatment per day for 3 days was optimal for MN induction.
Acridine Orange↗
The cta3+ gene that encodes a cation-transporting P-type ATPase is induced by salt stress under control of the Wis1-Sty1 MAPKK-MAPK cascade in fission yeast.
In Schizosaccharomyces pombe, the Wis1-Sty1 MAP (mitogen-activated protein) kinase signaling cascade is known to play a major role in cellular adaptation to adverse external stimuli, including osmotic stress, oxidative stress, nutrient deprivation, DNA-damaging agents, and heat stress. Nonetheless, it is not known whether or not this particular MAPK cascade is also involved in response to the most common stress, salinity. In this study, we provide evidence that the Wis1-Sty1 MAP cascade is implicated in salt stress response through regulating expression of a salinity-inducible gene. The downstream target gene thus identified is the cta3+ gene, which encodes a cation-transporting P-type ATPase. The salt stress-responsive nature of cta3+ expression was characterized extensively. It was found that not only the Sty1 MAP kinase but also the Atf1 transcription factor is crucial for the inducible expression of cta3+. As far as we know, this is the first instance that the stress-activated Wis1-Sty1 MAPK cascade plays a role in salt stress response in S. pombe.
Adenosine Triphosphatases↗
Retraction: absence of human T-cell lymphotropic virus type I in cutaneous T-cell lymphoma.
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Retraction Notice↗
Nitric oxide induces apoptotic death of cardiomyocytes via a cyclic-GMP-dependent pathway.
Recently, we have reported that excess amounts of nitric oxide (NO) produced by inducible NO synthase are involved in the development of myocardial damage in rats with induced myocarditis. However, there remain many problems to be solved concerning its mechanism of action. In this study, we examined whether NO induces apoptotic cell death in cardiomyocytes. Cultured neonatal rat cardiomyocytes were exposed to S-nitroso-N-acetylpenicillamine (SNAP) and (+/-)-E-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexeneamine (NOR 3), as NO donors, or 8-bromo-cyclic GMP (cGMP), an analog of cGMP which functions as a second messenger in cells stimulated by NO. DNA fragmentation was confirmed by electron microscopy, by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) method, and by agarose gel electrophoresis. Exogenously supplied SNAP or NOR 3 induced cardiomyocyte apoptosis in a dose- and time-dependent manner. Cardiomyocytes exposed to SNAP displayed typical features of apoptosis as demonstrated by electron microscopy. Treatment of the cells with 8-bromo-cGMP also induced apoptosis. In cardiomyocytes, SNAP-induced apoptosis was completely blocked by a PKG inhibitor (KT5823) and by a soluble guanylate cyclase inhibitor (ODQ) and was suppressed by hemoglobin and was completely blocked by ZVAD-FMK, a caspase inhibitor. These results show that NO-mediated apoptosis of cardiomyocytes is cGMP dependent and that caspases are involved in this process.
Animals↗
Tense blisters after bone marrow transplantation.
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Biopsy↗
Desmoglein ELISAs: a novel diagnostic tool for pemphigus.
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Autoantibodies↗
Desmoglein 1 and desmoglein 3 are the target autoantigens in herpetiform pemphigus.
OBJECTIVE: To determine the cell surface autoimmune target of herpetiform pemphigus (HP). DESIGN: Serum samples of HP were examined by immunoblot studies with human epidermal extracts, enzyme-linked immunosorbent assay with baculovirus-expressed recombinant desmoglein (rDsg) 1 and rDsg3, and immunoadsorption assay with rDsg. PATIENTS: Twenty serum samples were obtained from patients with HP who have typical clinical and histological features. All serum samples showed positive staining against keratinocyte cell surfaces by indirect immunofluorescence studies with healthy human skin. RESULTS: Immunoblot results showed that of 17 HP serum samples, only 5 reacted with a 160-kd band and 1 reacted with a 130-kd band. Results of enzyme-linked immunosorbent assays with rDsg1 and rDsg3 demonstrated that of 20 HP serum samples, 16 were positive against Dsg1 and 4 were positive against Dsg3. No serum samples reacted with both. Furthermore, in 19 of 20 HP serum samples, immunoreactivity against keratinocyte cell surfaces was completely removed by preincubation with rDsg1 and rDsg3 as shown by indirect immunofluorescence, excluding a possibility that these HP sera contain autoantibodies against other cell surface molecules. CONCLUSIONS: Dsg1 and Dsg3 are the major cell surface target molecules of HP, suggesting that most cases of HP are clinical variants of pemphigus foliaceus and that the rest might be variants of pemphigus vulgaris.
Autoantigens↗
Ultrastructural features of the myocardium of children with dilated cardiomyopathy.
We analyzed the electron-microscopic features of endomyocardial biopsy from pediatric patients with dilated cardiomyopathy (DCM). The specimens examined were taken from the right ventricle of ten patients aged from 2 to 15 years (mean 9.7 years). Biopsy specimens from eight patients with congenital heart disease (tetralogy of Fallot), aged from 3 to 12 (mean 7.3 years), and ten adult patients with DCM, aged from 32 to 60 (mean 45 years), were also examined. Patients considered to have endocardial fibroelastosis, arrhythmogenic right ventricular cardiomyopathy, specific cardiomyopathy, or coronary heart disease were excluded from this study. Specimens from pediatric patients with DCM showed various degrees of ultrastructural abnormalities of myocytes, including myofibrillar fragmentation, mitochondrial abnormalities, and intracellular edema. The ultrastructurally determined contractility failure index based on the severity of myocardial degeneration at the electronmicroscopic level was 4.9 +/- 1.1. This value was significantly higher than that in patients with tetralogy of Fallot (0.9 +/- 0.6, P < 0.001) but was not significantly different from that in adult patients with DCM (6.1 +/- 2.6). The index of pediatric patients with DCM who died within 3 years was high (6.0 +/- 0.8). Basal lamina layering of a capillary (BLL) in the myocardium was revealed in 1 of the 10 (10%) pediatric patients with DCM and in 6 of the 10 (60%) adult patients with DCM (P < 0.05). No BLL was noted in the patients with tetralogy of Fallot. These findings may be related to the pathogenesis of DCM in children and adults.
Adolescent↗
Oral clonidine premedication reduces induction dose and prolongs awakening time from propofol-nitrous oxide anesthesia.
PURPOSE: To evaluate whether oral clonidine premedication affects the induction dose of propofol and awakening time from epidural and propofol anesthesia. METHODS: Thirty-nine female patients (ASA I or II) were randomly allocated to receive 5 microg x kg(-1) clonidine p.o. or no clonidine 90 min before induction of anesthesia. After epidural anesthesia was achieved with lidocaine, general anesthesia was induced with continuous i.v. infusion of propofol at a rate of 50 mg x min(-1) until loss of eyelash reflex and responses to verbal commands, which were judged by a blinded observer. After a laryngeal mask airway was inserted, anesthesia was maintained with N2O 67%, O2 33% and propofol adjusted to maintain hemodynamic stability. After completion of surgery, a blinded observer recorded the time from discontinuance of propofol and N2O until the patient was awake and responsive (awakening time), and then, the laryngeal mask airway was removed. RESULTS: The induction dose of propofol in the clonidine group (1.4 +/- 0.3 mg) was less than that in the control group (1.9 +/- 0.4 mg, P < 0.05), while the awakening time of the clonidine group (470 +/- 145 sec) was longer than that of the control group (329 +/- 123 sec, P < 0.05). CONCLUSION: Premedication with 5 microg x kg(-1) clonidine p.o. reduced the induction dose of propofol, but delayed emergence from propofol anesthesia.
Adrenergic alpha-Agonists↗
A molecular phylogeny of Lilium in the internal transcribed spacer region of nuclear ribosomal DNA.
Phylogenetic relationships among 55 species of Lilium, Cardiocrinum giganteum, and Nomocharis saluenensis were inferred from nucleotide sequence variations in the internal transcribed spacer (ITS) regions of 18S-25S nuclear ribosomal DNA. The phylogeny derived from ITS sequences estimated using maximum-likelihood methods indicated that (1) most of the species construct their own clade according to the classification based on morphological features at the section level; (2) section Daurolirion is not independent of Sinomartagon, and it is appropriate to integrate two sections as Sinomartagon; (3) it is appropriate that L. henryi and L. bulbiferum are classified into subsection 6a and Sinomartagon-Daurolirion, respectively; (4) subsection 6b is much closer to Sinomartagon than subsection 6a and Archelirion, and it arose directly from Sinomartagon; and (5) Lilium is much closer to Nomocharis than Cardiocrinum. Phylogenetic estimation using sequences of the ITS region is suitable at the levels of genus, section, and most of subsection.
Base Sequence↗
Deletion in the beige gene of the beige rat owing to recombination between LINE1s.
We have determined the molecular genetic basis of the rat beige mutant, a model for human Chediak-Higashi syndrome. Deletion of a 578-bp sequence, which led to a frame shift and a presumably non-functional truncated BEIGE protein, was identified in beige cDNA. The beige rat had a deletion of about 20 kb of genomic DNA, including three exons, which constitute the deleted 578-bp cDNA fragment. LINE1s (Long Interspersed Nucleolar Element 1) were identified at the site of the deletion. Consensus recognition sequences for DNA topoisomerase I were clustered at the putative deletion junction sites in LINE1s. We conclude that the deletion in the beige gene mediated by recombination between LINE1s is the causative mutation in the beige rat. The recombination might have been induced by DNA topoisomerase I and the extensive sequence homology between LINE1s.
Amino Acid Sequence↗
Expression of plectin and HD1 epitopes in patients with epidermolysis bullosa simplex associated with muscular dystrophy.
Plectin, a widespread cytoskeletal linker protein, is prominently expressed in basal keratinocytes of the epidermis. HD1, originally identified as a hemidesmosomal protein, has been suggested to be an isoform of or closely related to plectin, but the exact relationship between these proteins is unknown. Plectin has recently been identified as the gene/protein system at fault in epidermolysis bullosa simplex associated with muscular dystrophy (EBS-MD; OMIM# 226670). In this study, we examined the expression patterns of plectin and HD1 epitopes in the skin of four unrelated patients with EBS-MD confirmed to be caused by plectin gene mutations. By indirect immunofluorescence, all monoclonal antibodies (mAbs) to plectin (5B3, 10F6) or to HD1 (121, E2, K15, 156) bound to the epidermal basement membrane zone (BMZ) of normal human skin. In addition, immunostaining along the periphery of keratinocytes was detected with mAbs 5B3, 10F6 (antiplectin), K15 and 156 (anti-HD1), but not with mAbs 121 and E2 (anti-HD1). Immunolabeling for mAbs 5B3 and 10F6 (antiplectin) was absent in the skin of three patients who had premature termination codon mutations in the plectin gene in both alleles. In contrast, labeling was only slightly reduced in a patient who was homozygous for a 9-bp in-frame deletion mutation in the same gene. Interestingly, peripheral labeling of keratinocytes using mAbs K15 and 156 (anti-HD1) was clearly present in all the patients despite the disappearance of BMZ labeling. Quantitative analysis by postembedding immunoelectron microscopy demonstrated that both plectin and HD1 epitopes were localized in the inner plaque of hemidesmosomes with a mean distance of 110 and 120 nm from the plasma membrane, respectively. These results confirm the molecular heterogeneity of EBS-MD in terms of the expression patterns of plectin and HD1 epitopes which correlate with clinical severity, the pattern of plectin gene mutations and their consequences.
Adult↗