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Biomedical subjects

A Tominaga

Publications and source records attributed to A Tominaga.

At least 37 records · Page 2Linked to original sources

Size-adjustable titanium plate for reconstruction of the sella turcica. Technical note.

A size-adjustable plate constructed of pure titanium is proposed for use in the reconstruction of the sella turcica. The plate is composed of two semicircular pieces that are connected by a hinge located at the top of the plate. Using an applicator, the plate is inserted into the sella turcica in a closed position. The same applicator is then used to open and secure the plate. The titanium causes minimal ferromagnetic artifacts on postoperative magnetic resonance imaging. Preliminary findings indicate a possible clinical use for this plate in the reconstruction of the sella turcica when no suitable piece of bone is available.

Adenoma↗

Spontaneous disappearance of a middle cranial fossa arachnoid cyst after suppurative meningitis.

BACKGROUND: Spontaneous disappearance of an arachnoid cyst is very rare, particularly after suppurative meningitis. CASE REPORT: A 2-month-old boy with a high fever was diagnosed with suppurative meningitis by cerebrospinal fluid examination. Computed tomography disclosed a large arachnoid cyst in the left middle cranial fossa. Two months later, the meningitis was cured. The arachnoid cyst disappeared with long-term antibiotic therapy alone. CONCLUSION: Although an infected arachnoid cyst may disappear with antibiotic treatment alone, careful observation and individualized patient management are essential.

Arachnoid Cysts↗

Trans-sellar color Doppler ultrasonography during transsphenoidal surgery.

OBJECTIVE: To improve the safety and efficacy of transsphenoidal pituitary adenoma surgery, we investigated transsphenoidal intraoperative color Doppler ultrasonography using a biplane transducer system. METHODS: We studied 23 patients with pituitary adenomas (18 patients with macroadenomas and 5 patients with microadenomas) who underwent transsphenoidal surgery. The Hitachi EUB555 color Doppler ultrasound system (Hitachi Medical, Tokyo, Japan) was used with a pediatric biplane transesophageal echo cardiography probe (EUP-ES533, 7.5 MHz, biplane phased array sector probe, 9.8-mm tip). The probe was inserted into the saline-filled sphenoid sinus after the sellar floor was opened. Intra- and suprasellar images were obtained just before dural incision and after the tumor removal was thought to have been accomplished. RESULTS: In all patients, the tumor was depicted as a slightly hyperechoic mass, as compared with the cerebrum. Using color Doppler imaging, major cerebral arteries were depicted clearly in 74% of patients. The pituitary glands, pituitary stalks, and optic chiasms were observed in patients with small adenomas, but not when large adenomas were present. Cavernous sinus invasion, concomitant aneurysm, and residual tumor were clearly visualized. In patients with large adenomas, the end point of surgery was decided when there was an ultrasonographically demonstrated collapsed tumor capsule, subcapsular total vacancy, and reappearance of the optic chiasm. CONCLUSION: Trans-sellar color Doppler ultrasonography seems to be a useful intraoperative guiding system that may improve the safety and efficacy of transsphenoidal surgery.

Adenoma↗

Effects of successful adenomectomy on body composition in acromegaly.

The purpose of the present study was to investigate postsurgical change in body composition in patients who have undergone surgery for acromegaly. Eight patients with acromegaly had determination of serum GH, insulin-like growth factor-I (IGF-I), height, body weight, and bioelectric impedance before surgery and at 2 weeks, 1 month, 3 months, and 6 months after surgery. Body composition was analyzed by bioelectric impedance analysis (BIA). We analyzed body fat (BF), body lean mass (BLM), body cell mass (BCM), total body water (TBW), intracellular water (ICW) and extracellular water (ECW). The serum GH concentration and IGF-I had decreased significantly 2 weeks after surgery. Body weight had decreased significantly 1 month after surgery and recovered 3 months after surgery. BIA showed that TBW and BCM had decreased significantly 2 weeks after surgery. BF gradually increased up to 1 month after surgery and was increased significantly at 3 months after surgery. The percent ratio of TBW/body weight decreased and the percent ratio of BF/body weight increased during the 6 months after surgery. The percent ratio of ECW/TBW did not change during the 6 months following surgery. In conclusion, the rapid body weight loss which occurred within 2 weeks after surgery was caused by decreases in TBW and BCM. The recovery of body weight, which was seen later than 1 month after surgery, was caused by an increase in BF. The postoperative change in body composition in acromegaly ceased 3 months after surgery.

Acromegaly↗

Effects of granulocyte/macrophage colony-stimulating factor on the development and differentiation of CD5-positive macrophages and their potential derivation from a CD5-positive B-cell lineage in mice.

In co-cultures of either the murine pre-B cell line J13, fetal liver cells, or adult peritoneal or bone marrow cells with ST2 mouse bone marrow stromal cells in the presence of granulocyte/macrophage colony-stimulating factor (GM-CSF), the development of CD5+ macrophages was demonstrated by immunohistochemical staining and flow cytometry. Although CD5+ macrophages were not present in the peritoneal cavities of normal mice, approximately 30% of the peritoneal macrophages in viable motheaten (mev/mev) mice, deficient in SHP-1 protein tyrosine phosphatase, expressed cell surface CD5 and B220, markers for B cells. In the mev/mev mice, GM-CSF level in peritoneal fluid was increased significantly. At 5 days after daily intravenous injection with GM-CSF, many CD5+ macrophages appeared in the peritoneal cavity and in omental milky spots of normal mice but fewer in osteopetrosis (op) mutant mice, deficient in macrophage (M)-CSF. These results indicate that GM-CSF, in combination with M-CSF, induces the development and differentiation of CD5+ macrophages in the peritoneal cavity, particularly in the omental milky spots of mice. In the peritoneal cavity of GM-CSF-treated mice, the percentages of hematopoietic progenitor cells doubly positive for CD5 and CD34 or c-kit and of macrophage precursor cells doubly positive for CD5 and ER-MP58 or ER-MP20 were increased significantly during the development of CD5+ macrophages and CD5 B cells, suggesting that CD5+ macrophages and B cells may share a bipotential progenitor in vivo.

Animals↗

Persistent infiltration of CD45RC- CD4+ T cells, Th2-like effector cells, in prolonging hepatic allografts in rats pretreated with a donor-specific blood transfusion.

A single intravenous injection of freshly heparinized blood from a donor-specific blood transfusion (DST) seven days before transplantation significantly prolongs the subsequent survival of hepatic allografts from ACI(RT1a) to LEW(RT1(1)) rats. We used W3/25 (anti-CD4) and OX22 (anti-CD45RC: an isoform of leukocyte-common antigen [CD45R]) monoclonal antibodies to investigate the cellular identity of hepatic allograft infiltrates following transplantation. The number of CD4+ and CD45RC+ cells in untreated allografts increased equally over time by day seven. However, in DST-treated hepatic allografts, CD4+ and CD45RC+ cells also increased over time by day 14, but the increment in the number of CD4+ cells was significantly greater than that in CD45RC+ cells. While the number of CD4+ cells remained persistently elevated in the hepatic allografts of rats pretreated with DST, they did not initiate rejection. Fluorescence-activated cell sorter (FACS) analysis revealed that the accumulated CD4+ T cells could be divided into two subsets, CD45RC- CD4+ and CD45RC+ CD4+ T cells, and that the ratio of CD45RC- CD4+/CD45RC+ CD4+ T cells in the hepatic allografts of recipients pretreated with DST was significantly greater than that in untreated allografts. Reverse-transcriptase polymerase chain reaction (RT-PCR) analysis demonstrated that CD45RC- CD4+ T cells expressed interleukin (IL)-4 and IL-10 messenger RNA (mRNA), but not IL-2 and interferon gamma (IFN-gamma). The pattern of messenger RNA expression in hepatic allograft infiltrates from animals pretreated with DST provides compelling evidence for the selective in vivo preservation of T-helper (Th2)-specific cytokines in the rat system. Our studies show that CD45RC leukocyte-common antigen expression can define different populations of hepatic infiltrating CD4+ T cells. A persistent infiltration of CD45RC- CD4+ T cells, Th2-like effector cells, is characteristic of hepatic allografts with a prolonged survival in DST-pretreated rats.

Animals↗

Usefulness of three-dimensional phase contrast MR angiography on arteriovenous malformations.

Prospective three-dimensional phase contrast (3D-PC) MR angiography was obtained in 34 patients with arteriovenous malformations (AVM) and comparison was made between digital substraction angiography (DSA) and three-dimensional time-of-flight (3D-TOF) methods. Velocity encoding (VENC) for 3D-PC was adjusted to 60 and 10 cm/sec., and was changed only when adequate information was not obtained. VENC 60 cm/sec, demonstrated the main feeders in 100% of cases and the nidus in 86% of cases whereas VENC 10 cm/sec. showed the draining vein in 78% of cases. The detection rate of feeder, nidus and drainer was 60%, 40% and 13% respectively by the TOF technique. The mean size of the nidus as compared with DSA as standard was 130% with MRI, 108% with 3D-PC and 92% with the TOF technique and this difference was not statistically significant. 3D-PC was clearly superior in detecting AVM in the presence of hemosiderin, hematoma or surgical clips. It also showed gradual disappearance of the lesion after radiosurgery. We found 3D-PC superior to 3D-TOF in the diagnosis, therapeutic planning and follow-up of AVM.

Adolescent↗

Incidence of intracranial aneurysm associated with pituitary adenoma.

The incidence of intracranial aneurysm associated with pituitary adenoma is not definitely established although reported higher than in general population. This study was designed to find the existence of such association in a large series of pituitary adenoma cases. A retrospective study of 467 cases of pituitary adenoma (mean age: 41 +/- 15 years) was done. All patients underwent cerebral angiography at least of anterior circulation, detailed hormonal study, and 155 cases had additional magnetic resonance (MR) angiography. Twenty-five cases (5.4%) of pituitary adenoma (mean age 52 years) had intracranial aneurysm, 97% on anterior circulation, and 12% had multiple aneurysms. Two cases presented with aneurysmal rupture and the rest were incidental. Aneurysm was more frequently seen with increasing age (p < 0.001) and the age distribution resembled that of aneurysm among general population. Although the combination was most frequent among nonfunctioning adenoma (8.8%), and least frequent among prolactinoma (2.4%), this association was again due to age factor. There was no association between hormone secretion, size and invasive nature of the tumor. The results showed no association between intracranial aneurysm and pituitary adenoma. Our speculation is that such occurrence is merely a chance factor and the risk is no greater than that among general population.

Adenoma↗

MIB1 immunopositivity is associated with rapid regrowth of pituitary adenomas.

Pituitary adenomas are generally regarded as benign tumours, but they may recur. We identified eight patients with pituitary adenomas that showed rapid regrowth within 2 years of initial surgery. We estimated the percentage of cells in each specimen that showed positive immunostaining for MIB1 (a novel anti-Ki-67) and compared the values to those of 40 adenomas that showed no regrowth. The mean MIB1 index for 40 adenomas that showed no evidence of regrowth was 0.19 +/- 0.06%. This was significantly (p < 0.0001) lower than that for adenomas that showed rapid regrowth (1.27 +/- 0.31%), based on the initial resected specimens. Immediately after detection of rapid regrowth and in adenomas that were resistant to bromocriptine or irradiation, the MIB1 index was always greater than 1.0%. Most patients with rapidly regrowing adenomas were well controlled by radiation therapy. Our results suggest that a MIB1 index greater than 1.0% may be a useful predictor of rapid regrowth of pituitary adenomas and may be useful for planning of therapy.

Adenoma↗

Expression of epithelial cadherin and cavernous sinus invasion in human pituitary adenomas.

Pituitary adenomas generally are regarded as benign tumors, although some invade the cavernous sinus and recur. We examined the epithelial cadherin (E-CD) expression in 30 pituitary adenomas (6 with cavernous sinus invasion and 24 without). Immunoreactivity of E-CD were found in all pituitary adenomas but they were very various. The presence of an association between E-CD expression and cavernous sinus invasion was assessed. There were no significant differences in E-CD expression between invasive and noninvasive adenomas. These results suggest that E-CD expression is not associated with cavernous sinus invasion in pituitary adenomas.

Adenoma↗

Cloning and characterization of the region III flagellar operons of the four Shigella subgroups: genetic defects that cause loss of flagella of Shigella boydii and Shigella sonnei.

To detect genetic defects that might have caused loss of flagella in Shigella boydii and Shigella sonnei, the region III flagellar (fli) operons were cloned from certain strains and analyzed with reference to the restriction maps and genetic maps of Escherichia coli fli operons. S. boydii NCTC9733 (strain C5 in this paper) had the 988-bp internal deletion in the fliF gene that encodes a large substructural protein of the basal body. Two strains (C1 and C8) had deletions of the entire fliF operon, and the remaining three (C3, C4, and C9) differed in the size of the restriction fragments carrying the fliF and fliL operons. Loss of flagella in S. boydii appears to originate in some defect in the fliF operon. S. sonnei IID969 lacked the fliD gene and, in place of it, carried two IS600 elements as inverted repeats. Genes downstream from fliD were not detected in the cloned fragment despite its large size but did appear elsewhere in the chromosome. The fliD gene encodes a cap protein of the flagellar filament, and its deletion results in overexpression of class 3 operons by the increased amount of FliA (sigmaF) caused by the excess export of the anti-sigma factor FlgM. Three other strains also had the fliD deletion, and two of them had another deletion in the fliF-fliG-fliH region. The fliD deletion might be the primary cause of loss of flagella in S. sonnei. The lack of FliF or FliD in each subgroup is discussed in connection with the maintenance of virulence and bacterial growth. We also discuss the process of loss of flagella in relation to transposition of IS elements and alterations of the noncoding region, which were found to be common to at least three subgroups.

Bacterial Proteins↗

Marked eosinophilia in interleukin-5 transgenic mice fails to prevent Trichinella spiralis infection.

In order to study the role of eosinophils in the host defense against Trichinella spiralis infection, worm recovery after infection with T. spiralis was compared between interleukin-5 transgenic (IL-5 Tg) mice with a constant high level of peripheral eosinophils and nontransgenic C3H/HeN mice. No significant difference in the recovery of muscle larvae or adult worms in the small intestine, fecundity of female adult worms, or infectivity of newborn larvae was observed between nonimmunized C3H/HeN and IL-5 Tg mice or C3H/HeN and IL-5 Tg mice immunized with somatic antigen of T. spiralis. However, a significant difference was observed in the fecundity of female adult worms and recovery of muscle larvae between nonimmunized and immunized IL-5 Tg mice or C3H/HeN mice. These results demonstrate that having more eosinophils does not improve immunity against the various aspects of T. spiralis infection.

Animals↗

Eosinophilia, IL-5 level and recovery of larvae in IL-5 transgenic mice infected with Toxocara canis.

Eosinophil counts, interleukin 5 (IL-5) concentrations in peripheral blood and larval recovery after infection with Toxocara canis were compared between IL-5 transgenic (Tg) and nontransgenic counterparts, C3H/HeN mice. In Tg mice characterized by a constant high level of peripheral eosinophils, eosinophils in peripheral blood fell to the lowest level on day 4 of a T. canis infection and then returned to the preinfection level on day 14. Serum IL-5 level fell to the lowest level on day 4 of infection, then recovered rapidly and peaked on day 14 postinfection. In contrast, the eosinophil and IL-5 levels in the peripheral blood peaked on days 11 and 7 of infection, respectively in C3H/HeN mice. The degree of eosinophil infiltration into the lung 4 days after infection was far more pronounced in Tg than C3H/HeN mice. The highest number of larvae recovered from the lungs of infected Tg and C3H/HeN mice occurred on day 4 postinfection. Strains of Tg and C3H/ HeN mice vaccinated with excretory and secretory (ES) antigens of T. canis larvae were infected with T. canis and the recovery of larvae on day 21 analysed. There were no significant differences in the mean number of larvae recovered from nonvaccinated Tg and C3H/HeN mice or vaccinated Tg and C3H/HeN mice. However, significant differences were demonstrated in the mean total number of larvae recovered from vaccinated and nonvaccinated Tg or C3H/HeN mice. These results suggest that immunocompetent cells other than eosinophils may play a significant role in the expulsion and killing of T. canis larvae in infected mice.

Animals↗

Two mechanisms for platelet-mediated killing of tumour cells: one cyclo-oxygenase dependent and the other nitric oxide dependent.

We have tried to identify the cytotoxic effectors in platelet-mediated tumour cell killing, using two tumour cell lines K562 (a chronic myelogenic leukaemic cell line) and LU99A (a lung cancer cell line), which are both sensitive to platelet cytotoxicity. Cyclo-oxygenase inhibitors, acetylsalicylic acid (ASA) and indomethacin, effectively inhibited the platelet-mediated killing of K562 cells, but not that of LU99A cells. In contrast, inhibitors of the nitric oxide (NO) pathway. NG-nitro-1-arginine (L-NA), haemoglobin and methylene blue, reduced the cytotoxic activity of platelets against LU99A, but not against K562. Synthetic analogues of platelet cyclo-oxygenase products thromboxane A2/ prostaglandin H2(TXA2/PGH2) exerted cytotoxicity against K562 cells but not against LU99A cells. Electron microscopic study showed that TXA2/PGH2 analogues induced bleb formation and disruption of the plasma membrane of K562 cells. K562 cells enhanced the production of TXA2 by platelets, as inferred from the accumulation of thromboxane B2 (TXB2), a spontaneous hydrolysis product of TXA2. LU99A cells had no such effects. These results indicate that platelets kill these two tumour cell lines through different mechanisms. In K562, the cyclooxygenase products TXA2/PGH2 possibly play a significant role but in LU99A the NO pathway seems to be involved.

Aspirin↗

Demonstration of a cross-talk between IL-2 and IL-5 in phosphorylation of IL-2 and IL-5 receptor beta chains.

We have examined phosphorylation mediated by cross-talk between growth signal pathways induced by IL-2 and IL-5. To analyze the phosphorylation process in the same cells, we established two sublines, T88-Mbeta1, which is a subline of a murine IL-5-dependent cell line, T88-M, by introduction of the human IL-2 receptor beta chain (IL-2Rbeta), and secondly CTLL-5Ralphabeta, which is a subline of a murine IL-2-dependent cell line, CTLL-2, by introduction of the murine IL-5 receptor alpha chain (IL-5Ralpha) and IL-5 receptor beta chain (IL-5Rbeta, betac) genes. Both T88-Mbeta1 and CTLL-5Ralphabeta expressed high-affinity receptors for IL-2 and IL-5, and proliferated in response to both factors. Tyrosine phosphorylation of IL-2Rbeta was induced by stimulation of T88-Mbeta1 with not only IL-2 but also IL-5. Anti-IL-2Rbeta-directed immune complexes from T88-Mbeta1 stimulated with IL-5 as well as with IL-2 contained an activated tyrosine kinase. However, stimulation with IL-5 but not IL-2 induced the tyrosine phosphorylation of IL-5Rbeta, betac, suggesting that IL-2 does not activate a tyrosine kinase which efficiently catalyzes the IL-5Rbeta molecule in response to IL-5. On the other hand, the detection of JAK1 and the other common set of phosphotyrosine-containing proteins after stimulation with either IL-5 or IL-2 suggests the existence of the same tyrosine phosphorylation pathways.

Animals↗

Detection and characterization of the flagellar master operon in the four Shigella subgroups.

Strains in the genus Shigella are nonmotile, but they retain some cryptic flagellar operons whether functional or defective (A.Tominaga, M. A.-H. Mahmoud, T. Mukaihara, and M. Enomoto, Mol. Microbiol. 12:277-285, 1994). To disclose the cause of motility loss in shigellae, the presence or defectiveness of the flhD and flhC genes, composing the master operon whose mutation causes inactivation of the entire flagellar regulon, was examined in the four Shigella subgroups. The flhD operon cloned from Shigella boydii and Shigella sonnei can activate, though insufficiently, the regulon in the Escherichia coli flhD or flhC mutant background. The clone from Shigella dysenteriae has a functional flhD gene and nonfunctional flhC gene, and its inactivation has been caused by the IS1 element inserted in its 5' end. The operon of Shigella flexneri is nonfunctional and has suffered an IS1-insertion mutation at the 5' end of the flhD gene. Comparison of restriction maps indicates that only the central 1.8-kb region, including part of the flhC gene and its adjacent mot operon, is conserved among the four Shigella subgroups as well as in E. coli, but in Salmonella typhimurium the whole map is quite different from the others. Motility loss in shigellae is not attributable to genetic damage in the master operon of a common ancestor, but it occurs separately in respective ancestors of the four subgroups, and in both S. dysenteriae and S.flexneri IS1 insertion in the master operon might be the primary cause of motility loss.

Chromosome Mapping↗