[Case of Cushing's syndrome due to bilateral adrenal adenomas with one presenting as melanotic adenoma].
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Adenoma↗
Biomedical subjects
A Sakamoto
Publications and source records attributed to A Sakamoto.
Delineation of genomic deletion in cardiomyopathic hamster.
Cardiomyopathic hamster is a representative animal model for autosomal recessive cardiomyopathy. We have previously shown that the transcript of delta-sarcoglycan is missing in the heart of cardiomyopathic hamster due to genomic deletion. Here we define the normal genomic region deleted in cardiomyopathic hamster, which spans about 30 kb interval and includes the two first exons of the delta-sarcoglycan gene. RNA blot analysis using genomic DNA fragments covering the entire deletion as probes failed to detect any transcript other than delta-sarcoglycan in normal hamster heart, suggesting that delta-sarcoglycan is the only transcript defective in the heart of cardiomyopathic hamster.
Animals↗
Expression of membrane type 1 matrix metalloproteinase, matrix metalloproteinase 2 and tissue inhibitor of metalloproteinase 2 in human cartilaginous tumors with special emphasis on mesenchymal and dedifferentiated chondrosarcoma.
Membrane type 1 matrix metalloproteinase (MT1-MMP) has been identified as an activator of the proenzyme of matrix metalloproteinase 2 (MMP-2: gelatinase A), and has also been shown to play a crucial role in tumor invasion by activating proMMP2 in both lung and gastric carcinoma. The tissue inhibitor of metalloproteinase 2 (TIMP-2) plus the MT1-MMP complex also plays an important role in the activation of proMMP-2. In this study, the expressions of MT1-MMP, MMP-2 and TIMP-2 were evaluated in 10 enchondromas, 34 conventional chondrosarcomas, 5 clear-cell chondrosarcomas, 7 mesenchymal chondrosarcomas and 8 dedifferentiated chondrosarcomas. The expressions were immunohistochemically visualized on paraffin sections and the levels of expression were assessed semiquantitatively. The extent of staining was assessed by the extent score in order to determine the overall level of expression. The extent scores of MT1-MMP, MMP-2 and TIMP-2 in grade 2 chondrosarcoma were significantly higher than those in either enchondroma or grade 1 chondrosarcoma (P < 0.05). In conventional chondrosarcoma, significant correlations were found between the extent scores of MT1-MMP and MMP-2 (P < 0.001), MT1-MMP and TIMP-2 (P < 0.01), and MMP-2 and TIMP-2 (P < 0.01). The undifferentiated small round tumor cells of mesenchymal chondrosarcoma showed lower positive rates and extent scores for MT1-MMP (2/7, 0.7 +/- 0.5) and MMP-2 (3/7, 0.7 +/- 0.4) than for cartilaginous components of mesenchymal chondrosarcoma [MT1-MMP (4/7, 1.3 +/- 0.5) and MMP-2 (7/7, 1.9 +/- 0.3)] or conventional chondrosarcoma. In dedifferentiated chondrosarcoma, the extent scores of MT1-MMP, MMP-2 and TIMP-2 in low-grade cartilaginous components were not significantly different from those in conventional chondrosarcoma; however, the high-grade anaplastic components showed high extent scores for MT1-MMP, MMP-2 and TIMP-2, compared with the low-grade cartilaginous components of dedifferentiated chondrosarcoma or conventional chondrosarcoma. According to our results, the expression of MT1-MMP as well as that of MMP-2 or TIMP-2 demonstrated a significant correlation with the tumor grade in human cartilaginous tumors. Furthermore, the expressions of MT1-MMP, MMP-2 and TIMP-2 were also found to play a crucial role in invasion in the high-grade components of dedifferentiated chondrosarcoma.
Bone Neoplasms↗
A comparative study of fibrous dysplasia and osteofibrous dysplasia with regard to expressions of c-fos and c-jun products and bone matrix proteins: a clinicopathologic review and immunohistochemical study of c-fos, c-jun, type I collagen, osteonectin, osteopontin, and osteocalcin.
Fibrous dysplasia and osteofibrous dysplasia are both benign fibro-osseous lesions of the bone and are generally seen during childhood or adolescence. Histologically, the features of these bone lesions sometimes look quite similar, but their precise nature remains controversial. We retrospectively studied clinicopathologic findings in 62 cases of fibrous dysplasia and 20 cases of osteofibrous dysplasia with regard to their anatomic location and histological appearance. From among these cases, the immunohistochemical expressions of c-fos and c-jun proto-oncogene products and bone matrix proteins of type I collagen, osteonectin, osteopontin, and osteocalcin were evaluated in 20 typical fibrous dysplasias and 17 osteofibrous dysplasias using paraffin sections, and these expressions were then assessed semiquantitatively. Microscopically, fibrous dysplasia showed various secondary changes, such as hyalinization, hemorrhage, xanthomatous reaction, and cystic change in 22 of the 62 cases (35%). This was a higher incidence than in osteofibrous dysplasia, in which only 2 of the 20 cases (10%) showed such changes. In the elderly fibrous dysplasia cases, the cellularity of fibroblast-like cells was rather low, and those cases were hyalinized. Almost all of the cases of fibrous dysplasia and osteofibrous dysplasia showed positive expressions of c-fos and c-jun products. The expressions of type I collagen and osteopontin showed no difference between fibrous dysplasia and osteofibrous dysplasia. Immunoreactivity for osteonectin in bone matrix was detected in only 1 case of fibrous dysplasia (1 of 20), whereas it was recognized in 14 of the 17 cases of osteofibrous dysplasia. Furthermore, the immunoreactivity for osteocalcin in bone matrix and fibroblast-like cells was higher in fibrous dysplasia than it was in osteofibrous dysplasia, semiquantitatively. Our immunohistochemical results regarding osteonectin and osteocalcin suggest that the bone matrix of fibrous dysplasia is somewhat more mature than that of osteofibrous dysplasia, and that the fibroblast-like cells in fibrous dysplasia share some phenotypic features with osteoprogenitor cells of normal osteogenic tissues. Fibrous dysplasia and osteofibrous dysplasia share some similar histological features, including c-fos and c-jun expressions, although different clinicohistologic features and immunohistochemical expressions of osteonectin and osteocalcin were observed. These features suggest that the mechanisms behind the development of fibrous dysplasia and osteofibrous dysplasia are similar, but this is not necessarily indicative of a closer relationship between the 2 diseases.
Adolescent↗
Characteristics of T-cell receptor Valpha24JalphaQ T cells, a human counterpart of murine NK1 T cells, from normal subjects.
BACKGROUND: In mice, natural killer (NK) T cells are specialized subsets of T cells that express an invariate T cell receptor (TCR) alpha chain and NK markers. In particular, murine NK1(+/-) T cells rapidly produce IL-4 and function as regulatory T cells. OBJECTIVE: We investigated the distribution of invariate TCR Valpha24JalphaQ T cells in CD4(-)CD8(-) double-negative (DN) and CD4(+) T cell populations of healthy individuals. We also studied the NK phenotypes and IL-4 production of Valpha24JalphaQ T cells. METHODS: The frequency of Valpha24(+/-) DN or CD4(+/-) T cells was determined by three-color FACS analysis, and subsequently the frequency of Valpha24JalphaQ rearrangement among Valpha24(+/-) DN or CD4(+/-) T cells was determined by sequencing. RESULTS: While the majority of DN Valpha24(+) T cells (68% to 88%) possessed TCR Valpha24JalphaQ, few of CD4(+) Valpha24(+) T cells (0.4% to 4%) did, indicating that Valpha24JalphaQ T cells are a major population of DN T cells, but not of CD4(+) T cells, in healthy subjects. The DN Valpha24JalphaQ T cells expressed a natural killer surface receptor NKR-P1A and CD56, but not CD16, on the cell surface. Moreover, DN Valpha24JalphaQ T cells promptly expressed IL-4 mRNA by stimulation with anti-Valpha24 monoclonal antibody in vitro. CONCLUSION: From these phenotypic and functional similarities of human DN Valpha24JalphaQ T cells with murine NK1(+) Valpha14Jalpha281 T cells, we conclude that DN Valpha24JalphaQ T cells are a counterpart of murine NK1(+) T cells, suggesting that they may play a regulatory role in autoimmune responses in vivo.
Animals↗
Enhanced tolerance to light stress of transgenic Arabidopsis plants that express the codA gene for a bacterial choline oxidase.
Arabidopsis thaliana was transformed with the codA gene from Arthrobacter globiformis. This gene encodes choline oxidase, an enzyme that converts choline to glycinebetaine. The photosynthetic activity, monitored in terms of chlorophyll fluorescence, of transformed plants was more tolerant to light stress than that of wild-type plants. This enhanced tolerance to light stress was caused by acceleration of the recovery of the photosystem II (PS II) complex from the photo-inactivated state. The transformed plants synthesized glycinebetaine, but no changes were detected in the relative levels of membrane lipids or in the relative levels of fatty acids in the various membrane lipids. Transformation with the codA gene increased levels of H2O2, a by-product of the reaction catalyzed by choline oxidase, by only 50% to 100% under stress or non-stress conditions. The activity of ascorbate peroxidase and, to a lesser extent, that of catalase in transformed plants were significantly higher than in the wild-type plants. These observations suggest that H2O2 produced by choline oxidase in the transformed plants might have stimulated the expression of H2O2 scavenging enzymes, with resultant maintenance of the level of H2O2 within a certain limited range. It appears that glycinebetaine produced in vivo, but not changes in membrane lipids or in the level of H2O2, protected the PS II complex in transformed plants from damage due to light stress.
Adaptation, Physiological↗
Prognostic value of nuclear morphometry in patients with TNM stage T1 ovarian clear cell adenocarcinoma.
In 40 patients with TNM stage T1 ovarian clear cell adenocarcinoma, we used nuclear morphometry to study the relations among morphometric variables, clinical prognostic factors and outcome. The presence of one or more giant nuclear cells was positively associated with death (OR = 10.6, P = 0.02) and tended to be associated with disease recurrence (OR = 5.1, P = 0.07). Nuclear irregularity (expressed in terms of the nuclear roundness factor) was positively associated with both death (OR = 8.6, P = 0.02) and disease recurrence (OR = 8.2, P = 0.02). A combination of giant nuclear cell presence or nuclear irregularity proved to be a useful prognostic indicator, with a sensitivity and specificity of 83% and 71% in the prediction of death, and 75% and 71% in the prediction of disease recurrence. Patients' age and substage were of no prognostic value. We conclude that the nuclear morphometric characteristics, especially the presence of giant nuclear cells and nuclear irregularity, may be useful in predicting outcome in patients with early stage ovarian clear cell adenocarcinoma.
Adenocarcinoma, Clear Cell↗
rAAV vector-mediated sarcogylcan gene transfer in a hamster model for limb girdle muscular dystrophy.
The limb girdle muscular dystrophies (LGMD) are a genetically and phenotypically heterogeneous group of degenerative neuromuscular diseases. A subset of the genetically recessive forms of LGMD are caused by mutations in the four muscle sarcoglycan genes (alpha, beta, gamma and delta). The coding sequences of all known sarcoglycan genes are smaller than 2 kb, and thus can be readily packaged in recombinant adeno-associated virus (rAAV) vectors. Previously, we have demonstrated highly efficient and sustained transduction in mature muscle tissue of immunocompetent animals with rAAV vectors. In this report, we utilize recombinant AAV containing the delta-sarcoglycan gene for genetic complementation of muscle diseases using a delta-sarcoglycan-deficient hamster model (Bio 14.6). We show efficient delivery and widespread expression of delta-sarcoglycan after a single intramuscular injection. Importantly, rAAV vector containing the human delta-sarcoglycan cDNA restored secondary biochemical deficiencies, with correct localization of other sarcoglycan proteins to the muscle fiber membrane. Interestingly, restoration of alpha-, as well as beta-sarcoglycan was homogeneous and properly localized throughout transduced muscle, and appeared unaffected by dramatic overexpression of delta-sarcoglycan in the cytoplasm of some myofibers. These results support the feasibility of rAAV vector's application to treat LGMD by means of direct in vivo gene transfer.
Animals↗
Effects of propofol anesthesia on cognitive recovery of patients undergoing electroconvulsive therapy.
The effects of different doses of propofol on post-electroconvulsive therapy (ECT) cognitive recovery were evaluated together with the effects on seizure duration and hemodynamic changes during ECT in 15 depressive patients. Propofol attenuated the increase in arterial blood pressure and heart rate in a dose-dependent manner compared with thiamylal. Propofol showed a clinically significant anticonvulsant effect during ECT in a dose-dependent manner. There were no significant differences among the four different induction groups in the mean recovery time from anesthesia, however, a low dose of propofol suppressed the early recovery of cognitive function. For early cognitive recovery after ECT, a deep anesthetic level is necessary when the traditional ECT apparatus is used which produces sine curve wave stimuli.
Adult↗
Early results of radical prostatectomy and adjuvant endocrine therapy for prostate cancer with or without preoperative androgen deprivation. The Prostate Cancer Study Group.
BACKGROUND: The effects of preoperative androgen deprivation were explored in the patients who received radical prostatectomy and subsequent adjuvant endocrine therapy for prostate cancer. METHODS: Stage A2, B or C prostate cancers were randomized to one of two groups: (i) group I (n=90), who received androgen deprivation (leuploride and chlormadinone acetate) for 3 months preoperatively followed by radical prostatectomy and adjuvant endocrine therapy (leuploride only); and (ii) group II (n=86), who underwent the surgery followed by 3 month androgen deprivation and subsequent adjuvant endocrine therapy. The effects of preoperative androgen deprivation on clinical relapse (serum prostate specific antigen (PSA) > 1.98 ng/mL, local recurrence or distant metastasis) and PSA relapse (PSA >0.2ng/mL) were evaluated at 2 years after randomization. RESULTS: There was no significant difference in clinical or PSA relapse-free survival and quality of life measures between the two groups, although relapses occurred significantly more frequently in patients who had more advanced stages, higher pretreatment PSA values or lower histologic differentiation in either group. Subgroup analysis indicated that clinical relapse-free survival in stage C cancer tended to be better in patients with preoperative androgen deprivation than in those patients without it (P< 0.1). CONCLUSIONS: Preoperative androgen deprivation may be beneficial for stage C prostate cancer patients receiving radical prostatectomy and adjuvant endocrine therapy over the 2 year observation period. A longer follow up is needed to clarify the exact extent of benefit in terms of survival and quality of life.
Aged↗
Characterization of the carboxyl terminal-truncated endothelin B receptor coexpressed with G protein-coupled receptor kinase 2.
The role of phosphorylation of the C-terminal tail of endothelin B receptor (ETBR) in agonist-induced desensitization was investigated, using a mutant lacking C-terminal 40 amino acids (delta 40 ETBR). In cells expressing the wild type or delta 40 ETBR, ET-1 caused rapid desensitization of calcium responses. The wild type ETBR was phosphorylated by biotinylated ET-1, and the phosphorylation was markedly enhanced by coexpression with G protein-coupled receptor kinase 2 (GRK2). However, delta 40 ETBR was not phosphorylated regardless of coexpression with GRK2. On the other hand, ET-1-induced IP3 formation in these cells was decreased by coexpression with GRK2 or catalytically inactive Lys220Arg GRK2 to the similar extent. The present study demonstrates the presence of phosphorylation-independent desensitization mechanism in delta 40 ETBR and suggests that GRK2 might play a role other than that as a kinase.
Animals↗
Endoscopic thoracic sympathectomy for primary erythromelalgia in the upper extremities.
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Adult↗
Epidermal growth factor-dependent dissociation of CrkII proto-oncogene product from the epidermal growth factor receptor in human glioma cells.
Human glioma cells frequently overexpress epidermal growth factor receptor (EGFR). We found that the CrkII proto-oncogene product was associated with the EGFR in human glioma cells in the absence of epidermal growth factor (EGF). EGF stimulation of glioma cells induced the phosphorylation of tyrosine 221 of the CrkII protein, which correlates with its dissociation from the EGFR. By contrast, Shc and Grb2 were inducibly associated with the EGFR in response to EGF stimulation of glioma cells. In A431 cells, epidermoid carcinoma cells which overexpress EGFR, CrkII was tyrosine-phosphorylated and associated with the EGFR in an EGF-dependent manner. Therefore, the dissociation of CrkII from the EGFR upon stimulation with EGF appears to be specific to glioma cells. The Cbl oncogene product was also tyrosine-phosphorylated in U87MG glioma cells upon EGF stimulation. However, unlike in other cell lines, CrkII was not inducibly bound to Cbl in U87MG glioma cells. Thus, EGF-dependent binding of CrkII to phosphotyrosine-containing proteins appears to be suppressed in glioma cells. To evaluate the physiological role of dissociation of CrkII from EGFR, we expressed the CrkII-23 mutant in glioma cells. CrkII-23 mutant, which was isolated as a suppressor gene of the EGF-dependent transformation of NRK cells, binds constitutively to EGFR. We found that expression of CrkII-23 inhibited the anchorage-independent growth of the glioma cells in the presence of EGF. Taken together, these data implicate EGF-dependent dissociation of CrkII from EGFR in the oncogenicity of human glioma cells.
Cell Adhesion↗
A new epileptic seizure classification based exclusively on ictal semiology.
Historically, seizure semiology was the main feature in the differential diagnosis of epileptic syndromes. With the development of clinical EEG, the definition of electroclinical complexes became an essential tool to define epileptic syndromes, particularly focal epileptic syndromes. Modern advances in diagnostic technology, particularly in neuroimaging and molecular biology, now permit better definitions of epileptic syndromes. At the same time detailed studies showed that there does not necessarily exist a one-to-one relationship between epileptic seizures or electroclinical complexes and epileptic syndromes. These developments call for the reintroduction of an epileptic seizure classification based exclusively on clinical semiology, similar to the seizure classifications which were used by neurologists before the introduction of the modern diagnostic methods. This classification of epileptic seizures should always be complemented by an epileptic syndrome classification based on all the available clinical information (clinical history, neurological exam, ictal semiology, EEG, anatomical and functional neuroimaging, etc.). Such an approach is more consistent with mainstream clinical neurology and would avoid the current confusion between the classification of epileptic seizures (which in the International Seizure Classification is actually a classification of electroclinical complexes) and the classification of epileptic syndromes.
Electroencephalography↗
Reduced blood flow in abdominal viscera measured by Doppler ultrasound during one-legged knee extension.
The redistribution of blood flow (BF) in the abdominal viscera during right-legged knee extension-flexion exercise at very low intensity [peak heart rate (HR), 76 beats/min] was examined by using Doppler ultrasound. While sitting, subjects performed a right-legged knee extension-flexion exercise every 6 s for 20 min. BF was measured in the upper abdominal aorta (Ao), right common femoral artery (RCFA), and left common femoral artery (LCFA). Visceral BF (BFVis) was determined by the equation [BFAo - (BFRCFA + BFLCFA)]. A comparison with the change in BF (DeltaBF) preexercise showed a greater increase in DeltaBFRCFA than in DeltaBFAo during exercise. This resulted in a reduction of BFVis to 56% of its preexercise value or a decrease in flow by 1,147 +/- 293 (+/-SE) ml/min at the peak workload. Oxygen consumption correlated positively with DeltaBFAo, DeltaBFRCFA, and DeltaBFLCFA but inversely with DeltaBFVis during exercise and recovery. Furthermore, BFVis (% of preexercise value) correlated inversely with both an increase in HR (r = -0.89), and percent peak oxygen consumption (r = -0.99). This study demonstrated that, even during very-low-intensity exercise (HR <90 beats/min), there was a significant shift in BF from the viscera to the exercising muscles.
Adult↗
Effects of temperature and preservation time on the pharmacological response of isolated vascular endothelial and smooth muscle function.
In clinical transplantation and cardiovascular surgery, cold preservation is usually used because it is a simple method. However, the established temperature is by no means exact. The aim of this study was to find the optimum storage temperature for preservation of the vasculature by observing the pharmacological endothelium and smooth muscle response. The thoracic aorta of 36 male Wister rats were studied in organ baths: as fresh control after 24 hours, 48 hours and 72 hours of storage at 0.5 degree C, 4 degrees C and 8 degrees C in Krebs-Henseleit bicarbonate (KHB) solution. Acetylcholine (Ach) was used to elicit endothelium-dependent relaxation, and sodium nitroprusside (SNP) to elicit smooth muscle-dependent relaxation. The contractility caused by Phenylephrine (Ph) was influenced by time but before 48 hours it was not influenced by preservation temperature. Significant responsive deterioration by Ach and SNP was seen after 24 hours of storage at 0.5 degree C as compared with storage at 4 degrees C. The endothelium-dependent relaxing function and smooth muscle-dependent relaxing function were best preserved at 4 degrees C and 8 degrees C. These results indicate that precise temperature control is necessary for vessel preservation in clinical situations.
Acetylcholine↗
Repeated propofol anesthesia for a patient with a history of neuroleptic malignant syndrome.
Neuroleptic malignant syndrome (NMS) is the most serious side effect produced by the administration of antipsychotic drugs. NMS shares many clinical similarities with malignant hyperthermia (MH), but the etiology of NMS and the relation between NMS and MH remain unknown. Anesthetic regimens for patients with NMS are not well established. We gave repeated anesthesia to a patient with a history of NMS undergoing electroconvulsive therapy for the treatment of depression. Propofol and vecuronium were used in twelve consecutive ECT sessions without complications. In this case report, we describe the safe and satisfactory repeated use of propofol in a patient with a history of NMS, and outline NMS and its questionable relation to MH.
Amoxapine↗
Structural basis of the function of endothelin receptor.
Endothelin receptor is a good model for analysis of the function of heptahelical G-protein coupled receptor. In ligand binding to the heptahelical receptor, the receptor has two functions, i.e. 'message' and 'address' functions. Each function has been assigned to different domain of the receptor. A different part of the ligand structure also corresponds to each domain of the receptor. Classically, classification of receptor has been done according to the difference of address domain, i.e. affinity difference of the receptor. However, present results predict that the classification of receptor is also possible according to the message domain. After stimulation of ET receptor by a ligand, the receptor transmits a signal to G-protein. Several kinds of G-proteins can possibly be activated. Different structural domains of the receptor are assigned to the coupling of the different Galpha-protein. Activated G-protein transmits the message to effector. Each Galpha-protein acts on different target molecules, resulting in different responses. However, the activation of each Galpha-protein presumably depends on its intracellular level. Even if the same receptor is activated with the same ligand, resulting final response is different from cell to cell. Therefore, classification of receptor according to the function of the receptor is difficult.
Animals↗