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Biomedical subjects

Y Yoshimoto

Publications and source records attributed to Y Yoshimoto.

At least 19 recordsLinked to original sources

Publication bias in neurosurgery: lessons from series of unruptured aneurysms.

BACKGROUND: Bias favouring publication of research with "positive" results over studies with "negative" results is widely suspected. The present investigation addressed this problem in the field of neurosurgery through a review of recent literature concerning outcome of surgery for unruptured intracranial aneurysms. METHODS AND FINDINGS: A Medline search was performed seeking case series of surgical treatment for unruptured intracranial aneurysms that analyzed 50 or more patients. Ten type I studies (retrospective studies from a single institution; 1457 patients) met these entry criteria. In general, type I studies reported excellent surgical outcome, with mean combined mortality and morbidity of 7.8% (95% confidence interval (CI), 6.4% to 9.2%). We found 4 multicenter or community-based studies (type II studies; 5401 patients). Mean combined mortality and morbidity in the type II studies was 20.3% (95% CI, 19.2% to 21.4%), much higher than in type I studies. Relative risk was 2.6 (95% CI, 2.2 to 3.1) for patients in type II studies compared with those in type I studies. Two meta-analyses (type III studies) described combined mortality and morbidity of 5.0% and 12.7%, essentially corresponding to results of type I studies. INTERPRETATION: Publication bias is present in the neurosurgical literature. Studies with an excellent surgical outcome are more likely to be published than those with an average outcome. Conclusions of literature reviews or meta-analyses based on published work therefore may be misleading. The solution to the problem would be community-based prospective registration of all patients who underwent surgery, providing a sampling frame free from publication bias.

Humans↗

Two starch-branching-enzyme isoforms occur in different fractions of developing seeds of kidney bean.

The nature and enzymic properties of starch-branching enzyme (SBE) are two of the dominant factors influencing the fine structure of starch. To understand the role of this enzyme's activity in the formation of starch in kidney bean (Phaseolus vulgaris L.), a study was undertaken to identify the major SBE sequences expressed during seed development and to characterize the enzymic properties of the coded recombinant enzymes. Two SBE cDNA species (designated pvsbe2 and pvsbe1) that displayed significant similarity (more than 70%) to other family A and B SBEs respectively were isolated. Northern blot analysis revealed that pvsbe1 and pvsbe2 were differentially expressed during seed development. pvsbe2 showed maximum steady-state transcript levels at the mid-stage of seed maturation, whereas pvsbe1 reached peak levels at a later stage. Western blot analysis with antisera raised against both recombinant proteins (rPvSBE1 and rPvSBE2) showed that these two SBEs were located in different amyloplast fractions of developing seeds of kidney bean. PvSBE2 was present in the soluble fraction, whereas PvSBE1 was associated with the starch granule fraction. The differences in location suggest that these two SBE isoenzymes have different roles in amylopectin synthesis in kidney bean seeds. rPvSBE1 and rPvSBE2 were purified from Escherichia coli and their kinetic properties were determined. The affinity of rPvSBE2 for amylose (K(m) 1.27 mg/ml) was lower than that of rPvSBE1 (0.46 mg/ml). The activity of rPvSBE2 was stimulated more than 3-fold in the presence of 0.3 M citrate, whereas rPvSBE1 activity was not affected. The implications of the enzymic properties and the distribution of SBEs and amylopectin structure are discussed.

1,4-alpha-Glucan Branching Enzyme↗

Hormonal regulation of the human ghrelin receptor gene transcription.

The aim of this study is to clarify the hormonal regulation of the human ghrelin receptor gene expression in GH(3) cells transfected with our previously cloned 5'-flanking region inserted into a luciferase reporter vector. Phorbor 12-tetradecanoate 13-acetate (TPA) with simultaneous addition of Bay K8644 mimicking ghrelin action caused a significant inhibition of the luciferase activity through the ghrelin receptor gene upstream proximal to -669 but not to -608 base pairs (bp). Glucocorticoid caused a weak but significant inhibition of the luciferase activity through the ghrelin receptor gene upstream proximal to -531 but not to -475 bp. Electrophoretic mobility shift assay resulted in binding of oligonucleotides between -669 and -640 bp, and between -520 and -491 bp to GH(3) cell nuclear proteins unlike AP(2) or glucocorticoid receptor. These results suggest that both TPA/Bay K8644 and glucocorticoid downregulate human ghrelin receptor gene expression through the transcriptional mechanism involving some nuclear factors.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

Injection of a sperm extract triggers egg activation in the newt Cynops pyrrhogaster.

Unfertilized eggs of the newt Cynops pyrrhogaster are arrested at the second meiotic metaphase. The primary signal for egg activation is a transient increase in [Ca2+](i), which is triggered by the fertilizing sperm and propagates over the egg cortex as a Ca2+ wave. We injected an extract of Cynops sperm (SE) into unfertilized eggs and induced a wave-like [Ca2+](i) increase which resulted in activation and resumption of meiosis. The SE-injected eggs showed degradation of cyclin B1 and DNA replication. When SE was boiled or treated with proteinase K before injection, it was unable to cause egg activation. Preinjection of Ca2+ -chelator BAPTA before SE injection inhibited egg activation. These results indicate that a heat-labile and proteinaceous factor in the sperm cytoplasm induces a transient increase in [Ca2+](i) which is required for egg activation. Injection of IP3 into unfertilized eggs caused an increase in [Ca2+](i) and egg activation, but injection of cADP-ribose did not. These results support the hypothesis that Ca2+ release at fertilization occurs via IP3 receptors.

Animals↗

Acute systemic inflammatory response syndrome in subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Systemic inflammatory response syndrome (SIRS) without infection is a well-known phenomenon that accompanies various acute cerebral insults. We sought to determine whether the initial SIRS score was associated with outcome in subarachnoid hemorrhage (SAH). METHODS: In 103 consecutive patients with SAH, the occurrence of SIRS was assessed according to the presence of >/=2 of the following: temperature of <36 degrees C or >38 degrees C, heart rate of >90 bpm, respiratory rate of >20 breaths/min, and white blood cell count of <4000/mm(3) or >12 000/mm(3). SIRS criteria and other prognostic parameters were evaluated as predictors of dichotomous Glasgow Outcome Scale score. RESULTS: SIRS was highly related to poor clinical grade (Hunt and Hess clinical grading scale), a large amount of SAH on CT (Fisher CT group), and high plasma glucose concentration on admission. By univariate analysis, the occurrence of SIRS was associated with higher mortality and morbidity rates than was the nonoccurrence (P<0.001). Among individual SIRS criteria, heart rate (P=0.003), respiration rate (P=0.003), and white blood cell count (P=0.03) were significant outcome predictors. By multivariate logistic regression analysis, the presence of SIRS independently predicted outcome. SIRS carried an increased risk of subsequent intracranial complications such as vasospasm and normal pressure hydrocephalus, as well as systemic complications. CONCLUSIONS: In SAH patients, SIRS on admission reflected the extent of tissue damage at onset and predicted further tissue disruption, producing clinical worsening and, ultimately, a poor outcome.

Acute Disease↗

[Reversible posterior leukoencephalopathy syndrome accompanied by HELLP syndrome and eclampsia: a case report].

We report a case of reversible posterior leukoencephalopathy syndrome accompanied by HELLP syndrome and eclampsia. A 30-year-old woman complained of diminution of visual acuity and eclampsia. Laboratory data revealed hemolysis, elevated liver enzyme and low platelets. CT showed low density areas in the bilateral occipital cortex. T1-weighted images showed a low signal intensity and T2-weighted images showed a high signal intensity in the occipital cortex bilaterally. Magnetic resonance angiography showed stenotic change in the intracranial artery. An operation was performed and significant improvement was seen in her visual function and MRI and MRA returned to normal on a month after operation. The mechanism of a reversible posterior leukoencephalopathy syndrome was discussed.

Adult↗

Lymph node metastases identified with mediastinoscopy in a patient with superficial carcinoma of the esophagus.

Superficial esophageal cancers limited to the lamina propria are not associated with lymph node metastases. Mediastinoscopic transhiatal esophagectomy was planned in a patient with widespread superficial cancer of the midthoracic esophagus. Sampling of the upper mediastinal lymph nodes revealed metastases. The operation was converted to a transthoracic esophagectomy with radical lymphadenectomy. Histopathologic examination of the resection specimen showed three metastatic lymph nodes, despite local invasion limited to the lamina propria. This is the first report of a patient with superficial esophageal cancer and lymph node metastases.

Carcinoma, Squamous Cell↗

Malignant struma ovarii with Graves' disease.

BACKGROUND: Malignant struma ovarii is a rare tumor, consisting of a struma ovarii with malignant change. Because of the rarity of the tumor, only a few reports with detailed data of thyroid function of the patient have been published. CASE: Medical and surgical treatments were performed in a case of malignant struma ovarii with Graves' disease and data from thyroid function tests were analyzed. After removal of the tumor, rapid improvement of thyroid function was observed and thyroglobulin level decreased. CONCLUSION: This case demonstrates the possible, if not dominant, contribution from the malignant struma ovarii to the hyperthyroidism of the patient.

Female↗

The expression of three types of CINCs by lipopolysaccharide-stimulated rat macrophages is inhibited similarly by anti-inflammatory steroids.

OBJECTIVE: Expression of CINCs was regulated differentially in lipopolysaccharide-stimulated rat macrophages. We examined whether the expression of CINCs in lipopolysaccharide-stimulated rat macrophages is similarly inhibited by anti-inflammatory drugs. MATERIALS AND METHODS: Rat peritoneal macrophages were stimulated by lipopolysaccharide in the presence of anti-inflammatory steroids (dexamethasone, prednisolone and hydrocortisone) or non-steroidal anti-inflammatory drugs (indomethacin and piroxicam). The production and mRNA expression of three types of CINCs were measured using enzyme-linked immunosorbent assay and northern hybridization. RESULTS: Anti-inflammatory steroids; dexamethasone, prednisolone and hydrocortisone, dose-dependently inhibited the production of CINC-1, -2 and -3, whose inhibitory patterns were similar to each other. Furthermore mRNA expression of each CINC was inhibited by dexamethasone in a dose-dependent manner. In contrast, non-steroidal anti-inflammatory drugs, indomethacin and piroxicam were without effect. Expression of each CINC was regulated differently; the production of CINC-1 reached a maximum at 12 h and then slightly decreased after lipopolysaccharide stimulation, whereas that of CINC-2 and CINC-3 increased up to 24 h. Dexamethasone inhibited the CINCs production and mRNA expression at 9 h after lipopolysaccharide stimulation. CONCLUSIONS: These results indicate no difference among CINC-1, -2 and -3 in the inhibition of production and mRNA expression of CINCs by anti-inflammatory steroids, although lipopolysaccharide differentially induces expression of each CINC expression in culture of rat macrophages.

Animals↗

8-bromo-cyclicAMP stimulates glucose transporter-1 expression in a human choriocarcinoma cell line.

Facilitative glucose transporter-1 (GLUT1) is abundant in trophoblast cells and is responsible for glucose transport in the placenta. However, the change in GLUT expression in human placenta upon trophoblast differentiation remains to be clarified. Therefore, we first examined the localization of GLUT1 and GLUT3 using human first-trimester chorionic villi. We found that GLUT1 and GLUT3 were mainly localized to syncytiotrophoblast and cytotrophoblast cells respectively. We analyzed whether placental GLUT1 and GLUT3 expression changes during differentiation using a human choriocarcinoma (BeWo) cell line which is known to show functional and morphological differentiation in response to cAMP in culture. Treatment of BeWo cells with 8-bromo-cyclicAMP (8-bromo-cAMP) increased the level of hCG secretion and induced cell fusion leading to the formation of large syncytia. Treatment of BeWo cells with 8-bromo-cAMP also resulted in a significant increase in glucose uptake on days 2-3 of culture. The stimulating effect of 8-bromo-cAMP on glucose uptake was concentration dependent. Northern and immunoblot analyses revealed that the levels of mRNA and protein of GLUT1, but not of GLUT3, were significantly increased by 8-bromo-cAMP. These findings suggest that 8-bromo-cAMP stimulates GLUT1 expression with differentiation in BeWo cells.

8-Bromo Cyclic Adenosine Monophosphate↗

Migrastatin, a new inhibitor of tumor cell migration from Streptomyces sp. MK929-43F1. Taxonomy, fermentation, isolation and biological activities.

A new compound, migrastatin, was isolated from a cultured broth of Streptomyces sp. MK929-43F1, as an inhibitor of tumor cell migration. It was purified by column chromatographies on silica gel and Sephadex LH-20 and HPLC. Migrastatin has the molecular formula of C27H39NO7 consisting of 14-membered macrolide and glutarimide moiety. It inhibited spontaneous migration of human esophageal cancer EC17 cells. Migration inhibitory activity of migrastatin was not dependent on cytotoxicity or inhibition of protein synthesis.

Animals↗

MK800-62F1, a new inhibitor of apoptotic cell death, from Streptomyces diastatochromogenes MK800-62F1. I. Taxonomy, fermentation, isolation, physico-chemical properties and biological activity.

A new compound, MK800-62F1, was isolated from a cultured broth of Streptomyces diastatochromogenes MK800-62F1. It inhibited H2O2-induced apoptosis in human small cell lung carcinoma Ms-1 cells as well as in human T-cell leukemia Jurkat cells. In addition, MK800-62F1 also inhibited camptothecin-induced apoptosis in Jurkat cells, which was mediated by intracellular H2O2 generation. MK800-62F1 did not exhibit antioxidative activity in vitro, suggesting that inhibition of apoptosis by MK800-62F1 was not due to the scavenging of H2O2, rather it was due to the modulation of the downstream event of H2O2 generation.

Antineoplastic Agents, Phytogenic↗

Secretagogue-induced exocytosis recruits G protein-gated K+ channels to plasma membrane in endocrine cells.

Stimulation-regulated fusion of vesicles to the plasma membrane is an essential step for hormone secretion but may also serve for the recruitment of functional proteins to the plasma membrane. While studying the distribution of G protein-gated K+ (KG) channels in the anterior pituitary lobe, we found KG channel subunits Kir3.1 and Kir3.4 localized on the membranes of intracellular dense core vesicles that contained thyrotropin. Stimulation of these thyrotroph cells with thyrotropin-releasing hormone provoked fusion of vesicles to the plasma membrane, increased expression of Kir3.1 and Kir3.4 subunits in the plasma membrane, and markedly enhanced KG currents stimulated by dopamine and somatostatin. These data indicate a novel mechanism for the rapid insertion of functional ion channels into the plasma membrane, which could form a new type of negative feedback control loop for hormone secretion in the endocrine system.

Amino Acid Sequence↗

Somatostatin induces hyperpolarization in pancreatic islet alpha cells by activating a G protein-gated K+ channel.

Somatostatin inhibits glucagon-secretion from pancreatic alpha cells but its underlying mechanism is unknown. In mouse alpha cells, we found that somatostatin induced prominent hyperpolarization by activating a K+ channel, which was unaffected by tolbutamide but prevented by pre-treating the cells with pertussis toxin. The K+ channel was activated by intracellular GTP (with somatostatin), GTPgammaS or Gbetagamma subunits. It was thus identified as a G protein-gated K+ (K(G)) channel. RT-PCR and immunohistochemical analyses suggested the K(G) channel to be composed of Kir3.2c and Kir3.4. This study identified a novel ionic mechanism involved in somatostatin-inhibition of glucagon-secretion from pancreatic alpha cells.

Acetylcholine↗

Characterization of G-protein-gated K+ channels composed of Kir3.2 subunits in dopaminergic neurons of the substantia nigra.

G-protein-gated K+ (KG) channels generate slow inhibitory postsynaptic potentials in the brain. Current opinion suggests that neuronal KG channels are heterotetramers of Kir3.1 and Kir3.2. In substantia nigra (SN), however, mRNA of Kir3.1 does not express, whereas that of Kir3.2 clearly does. Therefore, we have characterized the KG channels containing Kir3.2 subunits in SN using biochemical and immunological techniques. We found that they were composed of only Kir3.2 subunits and did not contain significant amounts of either Kir3.1 or Kir3.3. Furthermore, at least some of the KG channels in SN were assemblies of the splicing variants Kir3. 2a and Kir3.2c. The channels were localized specifically at the postsynaptic membrane on the dendrites of dopaminergic neurons. Kir3. 2c, but not Kir3.2a, could bind a PDZ domain-containing protein, PSD-95. The heterologously expressed KG channels composed of Kir3.2a plus Kir3.2c or Kir3.2a alone were activated by G-protein stimulation, but expression of Kir3.2c alone was not. This study reveals that the Kir3.2 splicing variants play distinct roles in the control of function and localization of some of the KG channels in dopaminergic neurons of SN.

Animals↗

A prospective study on the effects of early surgery on vasospasm after subarachnoid hemorrhage.

BACKGROUND: To test the hypothesis that early surgery prevents vasospasm, a prospective analysis used strictly selected cases of anterior communicating artery aneurysms with symmetric distribution of subarachnoid hemorrhage. METHODS: Seven patients underwent early surgery (9-29 hours after ictus) through a standard pterional approach. Subarachnoid blood clots surrounding the ipsilateral major cerebral arteries were meticulously irrigated and suctioned. Comparison was made between the hemispheres with surgical intervention and those without, in terms of incidence of delayed ischemic neurologic deficits and cerebral infarction on computed tomographic scans, degree of angiographic vasospasm, and cerebral blood flow (CBF). RESULT: The degree of angiographic vasospasm, quantified by measuring the alterations in the ratio of the diameters of the intracranial arteries (C1, M1) to the extracranial internal carotid artery (C5), did not differ significantly between the surgical and nonsurgical sides. The mean CBF was also comparable between both sides in the chronic spasm phase (Day 6-9) as well as in the early postoperative period (Day 1-3). A significant reduction of CBF was observed during the early postoperative period in the basal frontal lobe of the surgical side. This CBF reduction seems to correspond to brain retraction. CONCLUSIONS: The results suggest that the effect of clot removal may be offset by the negative aspect of early surgery, and early surgery per se seems to have little effect on the course of the chronic vasospasm.

Adult↗